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D elayed recovery . Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics PhD ( physio ) Mahatma Gandhi Medical college and research institute , puducherry , India . De finition . Recovery by definition is “to regain possession of”.

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d elayed recovery

Delayed recovery

Dr. S. Parthasarathy

MD., DA., DNB, MD (Acu),

Dip. Diab.DCA, Dip. Software statistics

PhD (physio)

Mahatma Gandhi Medical college and research institute , puducherry , India

de finition
  • Recovery by definition
        • is “to regain possession of”.

Whatever it is !!

i n anaesthesia
In anaesthesia
  • It is the same
  • It is usually and conventionally ascribed to General anesthesia
w hat is the dynamics
What is the dynamics ??
  • It is a spectrum of clinical condition varying
  • from a patient who has undergone a coronary surgery shifted on a ventilator
  • to a patient who underwent a curettage going home in two to three hours
w hen to say delayed recovery
When to say delayed recovery ??
  • If a patient does not generate a meaningful, directed response to ordinary levels of verbal or tactile stimuli within 30 minutes of PACU admission, he or she is exhibiting prolonged unconsciousness that requires a differential diagnosis.
d efinition of delayed recovery
Definition of delayed recovery
  • Intriguing
  • . It can be simply stated that when the patient does not recover when he is supposed to.
  • The mode of recovery may vary with the technique of anesthesia used like intravenous, inhalational or using neuromuscular blockers.
response to external stimulus
Response to External Stimulus
  • Sharp loud voice telling the first name
  • Tactile stimuli
  • Pinch and pain but no physical injury
  • Trapezius squeeze test
w hy we need to do better
Why we need to do better ??
  • shorter-acting intravenous agents
  • lower solubility inhalational anesthetics,
  • and the use of depth of anesthesia indicators, such as end-expired volatile agents ,processed EEG monitoring.
i nduction and recovery differences
Induction and recovery- differences
  • First, on induction the effect of solubility to hinder the rise in alveolar anesthetic concentration could be overcome by increasing the inspired anesthetic concentration–
  • the inspired concentration cannot be reduced below zero
  • Second, on induction all the tissues initially have the same anesthetic partial pressure-zero. On recovery the tissue partial pressures are variable.
causes of prolonged unconsciousness after anesthesia
Causes of Prolonged Unconsciousness After Anesthesia
  • Residual sedation from opioids
  • Residual sedation from inhalational agents
  • Residual sedation from premedications antiemetics
  • Hypercarbia or hypocarbia
  • Hypoxemia
  • Hypothermia
  • Cerebral hypoperfusion
  • Hypoglycemia or hyperglycemia
  • Hyperosmolar or hypoosmolar states
  • Coexisting medical illness
  • Central neurologic events
basic care
  • Airway – maintain a clear airway , give O2 reintubate if indicated
  • Breathing:- Ensure adequate respiration. If indicated ventilate the patient effectively via an endotracheal tube. Monitor SpO2.
  • Circulation:- Assess blood pressure, heart rate, ECG, Peripheral perfusion, conscious level and urine output. Resuscitate as indicated

Continue basics before steps for evaluation

  • Continue basics before steps for evaluation
  • Continue basics before steps for evaluation
a pproach step 1
Approach - Step 1
  • Vaporisers switched off
  • Back flown drugs in the IV set removed
  • Change the breathing circuit
  • Check the machine and gas sources
s tep 2
Step 2
  • The history, investigations and peri operative management including anaesth. chart and the timings of drug administration are analysed to spot a possible cause.
take special note of preexisting medical conditions
Take special note of preexisting medical conditions
  • cerebral vascular disease, transient ischemic attacks, stroke, intracranial tumor, cerebral aneurysm, or previous head trauma.
  • The presence of supraventriculardysrhythmias such as atrial fibrillation or flutter should lead one to consider the possibility of cerebral thromboembolism
take special note of preexisting medical conditions contd
Take special note of preexisting medical conditions --- contd
  • . A history of congenital heart disease, septal defect, endocarditis, or heart murmur may point toward paradoxical cerebral embolization with thrombus, vegetations, air, or fat.
  • Cirrhosis, chronic hepatitis, or other disorders of liver function may indicate an element of hepatic encephalopathy.
  • medications on a chronic basis
i ntra op events
Intra op events
  • intraoperative events such as transient airway obstruction,
  • periods of low arterial oxygen saturation
  • prolonged decreases in systemic blood pressure, dysrhythmias,
  • or blood loss
i ntra op events1
Intra op events
  • Level of responsiveness before induction
  • Extreme or unusual intraoperative positioning
  • Interventions near the cerebral circulation
i ntra op events2
Intra op events
  • Intracerebral structures can be damaged during sphenoid sinus procedures or middle ear procedures
  • In patients with facial fractures or those who have undergone transsphenoidal surgery, the inadvertent passage of nasogastric or nasotracheal tubes through the cribiform plate into the intracranial cavity can obviously produce severe brain injury intraoperatively.

Midazolam is metabolized by the same P450 iso-enzyme as alfentanil, such that co administration prolongs the actions of both drugs.

step 3
STEP – 3
  • 100% O2 for 10 – 15 minutes
  • IPPV
  • Hyperventilation
  • Forced diuresis
step 4
STEP – 4
  • Forced air warming with warm air blankets (Bair hugger) or similar device is the most effective method.
  • However wrapping in blankets and/or in foil sheets, ensuring the room is kept warm, and giving warm IV fluids, will all help.
step 5
STEP – 5


  • Hypoglycemia:
  • Can occur in small children and those who have been given insulin or oral hypoglycaemic drugs. It may also occur in liver failure, in the presence of alcohol excess and in septicaemia and malaria.
h ypoglycemia
  • Diabetes, Starvation
  • Alcohol, Sepsis
  • Liver failure, Paediatrics
  • Sulphonylureas, Endocrine tumours
  • Hypo adrenalism
s tep 5 continued
Step 5 - continued




May occur in decompensated diabetics i.e., hyperosmotic hyperglycaemic diabetic coma, or diabetic ketoacidosis

h yperglycemia
  • Ketoacidosis
  • Hyperosmolar non ketotic acidosis (HONK)
  • Lactic acidosis
  • Gestational diabetes
  • Insulin resistance (acromegally, Cushing’s)
  • Pancreatitis
step 5 continued
Step 5 - continued
  • This may be secondary to the underlying illness or as a consequence of the surgical procedure e.g., hyponatraemia occurring with trans-urethral resection or prostate (where glycine or other hypotonic fluid is used for irrigation).
step 6
STEP – 6
  • NALOXONE 1 to 4 µg/kg IV, promptly reverses opioid-induced analgesia and depression of ventilation. The short duration of action of naloxone (30 to 45 minutes.
  • flumazenil is 0.2 mg (8 to 15 µg/kg), which typically reverses the CNS effects of benzodiazepine agonists within about 2 minutes.
  • duration of action of flumazenil is 30 to 60 minutes,
  • continuous low-dose infusion of flumazenil, 0.1 to 0.4 mg/hour.
reversal agents
Reversal Agents
  • There are no specific reversal agents available to barbiturates, propofol, phenothiazines, and butyrophenones.
  • The administration of intravenous physostigmine (1.25 mg) generates a degree of central arousal that can counteract, but not reverse, depression from sedatives, antiemetics, and other depressant medications such as baclofen
opioid narcosis
opioid narcosis -
  • pin point pupils and slow respiratory rate. In this situation a test dose of naloxone may be given: iv increments of 100 to 200 micrograms are usually sufficient
c ombination
  • Sedatives , narcotics, minimal agent with hypercapnia just post op
can happen from back centrineuraxial
Can happen from back- (centrineuraxial)
  • The inadvertent subarachnoid injection of local anesthetic in epidural
  • high concentrations of local anesthetic directly into the intracranial cerebrospinal fluid
  • Epidural opioid --- subarachnoid === conscious status ??
step 7
STEP – 7
  • Residual neuromuscular blockade results in paralysis, which may be perceived as unresponsiveness though the patient may be fully conscious and aware.
  • NMJ monitoring
t hree problems
Three problems
  • Scoline apnea
  • Excess relaxants
  • Normal dose but more action
  • myasthenia gravis, muscular dystrophies, renal or hepatic diseases , amino glycosides
practice point relaxants
  • Avoid excessive doses of relaxants.
  • Intermediate acting drugs such as atracurium or vecuronium are easier to use than long acting ones.
  • Only give repeat doses when necessary (when there is evidence of muscle activity).
  • When giving repeat doses use 20-25% of the initial dose.
  • Wherever possible use a NMJ monitor to guide doses and assess reversal.
step 8
STEP – 8
  • Steroids
  • Thyroxin
  • Proteins
  • Antibiotics,
  • Fresh blood
t hese can also be reasons
These can also be reasons
  • Porphyrias
  • Hunter s syndrome
  • OSAS
  • Hypothyroid
  • Mucopolysacharidoses
central anticholinergic syndrome
Central anticholinergic syndrome
  • follow the use of anticholinergic drugs especially hyoscine, but also antihistamines, antidepressants, phenothiazines and pethidine.
  • physostigmine 0.04mg/kg slowly iv which acts within 5 minutes, but features may return after 1-2 hours.
step 9
STEP – 9
  • CT brain or anything suggested
  • In trauma patients or those requiring emergency surgery, the possibility of unrecognized head injury, asphyxia, or exposure to carbon monoxide, environmental toxins, or ingested poisons should be evaluated.
What Should Be Done When a Previously Responsive Patient Develops the Acute Onset of Unconsciousness?
  • Renarcotization,” “bi-phasic responses to opioids,” or “recurarization” are Untrue words and reasons
g oes back again
Goes back again ??
  • Medication-induced loss of consciousness can occur in a postoperative patient
  • IV tubing flushing
  • CNS dysfunction
a bnormal position can lead on to
Abnormal position can lead on to --
  • surgery is performed in the sitting position, especially with extreme flexion of the neck
  • Compression of the carotid arteries from external contact or a hematoma in the neck can also impede cerebral perfusion, particularly in patients with severe cerebrovascular disease.
don t compress neck
Don’t compress neck
  • Intraoperative interference with cerebral venous return instigated by external compression of the jugular veins, high intrathoracic pressures, jugular venous cannulation, or extreme head and neck positioning can lead to cerebral edema, increased intracranial pressure, and cerebral hypoperfusion.
spurious unconscious state
spurious unconscious state
  • Differentiating between an actual and spurious unconscious state is a clinical challenge.
  • In a supine patient who is feigning unconsciousness, dropping the patient's hand toward the face will often result in the arm falling to the side rather than toward the nose as gravity would normally direct it.
  • Bispectral index
diabetes insipidus
diabetes insipidus
  • Delayed recovery from general anaesthesia
  • Case report
  • Possible cause = diabetes insipidus
  • Anaesthesia – 1988 – vol 43 – 1073
o ther issues
Other issues
  • medical risk and expenditure of resources
  • Staff
  • Cost
c linical tricks
Clinical tricks
  • unresponsiveness may be due to Deafness
  • Tell them to breathe – sometimes apneic spell are reversed with this
  • Language – know to ask in patients known language

100% Oxygen, airway adjuncts,

manual ventilation

Assess ABC

GCS – stimulate



History, drugs , chart

Glucose, temperature


Correct hypoxia, hypercapnia or

Acidosis , electrolytes

Arterial blood gas analysis

CT head – consider

Clinical , tests

Where ? Dissociative test

we need to work
We need to work