Awareness Anaphylaxis MH Airway algorithms Flashcards
Q2 — Accidental awareness
a) What is accidental awareness under general anaesthesia
(AAGA)?
Awareness is said to have occurred when the patient has an explicit recall of the intraoperative events associated with or without pain.
b) What is the overall incidence of awareness under general
anaesthesia and the estimated awareness incidence for a
caesarean section under general anaesthesia as per the NAP5
study?
● The overall incidence of patients reporting an incidence of awareness under general anaesthesia is around 1:19,000.
● The estimated awareness incidence in a caesarean section under general anaesthesia is around 1:670 patients.
c) List the monitoring devices that can be used to help reduce the incidence of awareness under general anaesthesia.
Bispectral Index and M-Entropy™ —
both provide a processed EEG as
a measure of cortical suppression.
They give a number (dimensionless
index) to be interpreted.
● Narcotrend®.
● aepEX® device —
uses auditory evoked potentials to derive the depth
of anaesthesia.
● Another technique is the isolated forearm technique.
d) What are the factors contributing to the increased incidence of awareness?
● Females > males — 65% vs. 35%, respectively.
● Obese category patients > other
(underweight, normal, overweight
and morbidly obese groups of patients)
categories.
● Surgical specialty — obstetrics (highest incidence), cardiothoracic
surgery (second highest).
● Phases of anaesthesia — induction phase (more common) >
maintenance phase > emergence phase.
● Induction agents — more common with thiopentone, etomidate,
ketamine and midazolam compared with propofol.
● More common with TIVA.
● Reported more with the use of neuromuscular blockers than without
them.
● Use of neuromuscular blockers, not monitoring their effects and no
reversal of neuromuscular blockers — all increase the risk of
awareness.
● It is more likely to happen in patients with a history of awareness
under general anaesthesia in the past.
● Other over-representations for awareness in the NAP5 study included
early middle-age adults, out-of-hours operating under general
anaesthesia and junior anaesthetists managing the case.
● Drug errors including failure of anaesthetic delivery, e.g. malfunction
of the TIVA pump.
● Inadequate administration of volatile anaesthetic agent.
e) How would you minimise the chances of awareness in
anaesthesia?
● Identify risk factors during the pre-assessment stage itself.
● Vigilance during anaesthesia — keep a watch on the physiological
parameters (HR, BP, RR, obvious movements, lacrimation).
● Minimise drug errors during anaesthesia.
● Supplementary doses of induction agent in cases of unexpected delay
in intubation, e.g. in a difficult intubation.
● Use of neuromuscular monitoring if neuromuscular blockers are used.
● Depth of anaesthesia monitoring if using a TIVA technique.
● Extra caution in certain surgeries prone to awareness, e.g. caesarean
section under general anaesthesia, cardiothoracic surgeries, etc.
BJA Article
Key pts
Patients that experience distress during AAGA are prone to PTSD.
Evidence-based therapeutic management strategies for
AAGA-induced PTSD have been constrained
by the relatively low incidence of AAGA.
Treatment with antidepressants in combination with cognitive behavioural therapy is frequently used to treat PTSD.
BJA article conclusions
Accidental awareness under general anaesthesia is associated
with ASD and PTSD in patients who experience distress,
such as paralysis and pain during the event.
However, evidence-based therapeutic management strategies for ASD and PTSD have been constrained
by the relatively low incidence of AAGA.
Thus, treatment strategies are based on extrapolations from patients with PTSD that is not associated with AAGA.
Because significant depression affects 30–50%
of patients diagnosed with PTSD,
drug treatment with antidepressants
in combination with cognitive behavioural therapy
can be especially helpful
All reports of AAGA should be taken very seriously and institutional guidelines should be in place to
follow the NAP5 awareness support pathway.
Anaesthetists should be aware of the
risk factors for AAGA and
choose their anaesthetic plan carefully,
especially regarding use of
neuromuscular blocking drugs and TIVA.
Future prevention research might study the effects of targeted psychological therapies in patients at risk for post-surgical PTSD.
Incidence
. It is well established that the incidence of AAGA is significantly higher in paediatric, obstetric, and cardiac anaesthesia
heavily skewed towards women
AAGA in the UK showed that 117 out of 159 (74%) of AAGA claims were from women, and two thirds were related to obstetric care.
sex susceptibility to AAGA or possibly, a reporting bias.
Secondary analysis of 26,490 patients in the
B-Unaware trial, BAG-RECALL trial,
and MACS trial revealed that patients
with a history of AAGA were
five times more likely to experience AAGA again
The incidence of AAGA in NAP5 (∼1 out of 19,600) was remarkably lower than in previous reports
Study actively sought to report their personal experience of AAGA via a secure online portal. The authors of NAP5 argued that the occurrence of AAGA reported to NAP5 may be more relevant in clinical practice
Risk factors
Obstetric patients 10-fold increase
Cardiothoracic patients and a 2.5-fold increase in
Female sex increased susceptibility as 91 out of 141 (65%) cases of AAGA involved female patients.
Obese patients were three times more likely to experience
Total intravenous anaesthesia was overrepresented in patients who experienced AAGA (18% in AAGA cases vs 8% overall)
Anaesthetic drug type,
or perhaps the use of anaesthetic drugs that are typically reserved for emergencies, increased the risk of AAGA.
Ketamine, etomidate and thiopental were used most often in the AAGA activity survey cohort
neuromuscular blocking drugs were used.
Importantly, monitoring and reversal of neuromuscular block were less frequent in those with AAGA.
Limited usage, the NAP5 investigators were not able to derive a meaningful statistical analysis between pEEG use and AAGA.
The patient’s experience of accidental awareness during general anaesthesia
Spontaneous reports of AAGA did not occur routinely after the precipitating event.
Only 47 out of 141 (33%) reports were made on the day of the surgery and less than half within the first 24 h.
Many patients first reported AAGA during preparations for a subsequent procedure, as patients became understandably anxious about having general anaesthesia
postoperative checks on patients and may explain the disparity between patients’ and anaesthetists’ reports of AAGA.
NAP5 found that in 47% of AAGA cases, the recall of AAGA was described in a neutral way, involving few isolated aspects of the experience, such as auditory and tactile memory.
other 53% of the AAGA events were associated with distress. The primary causes of distress were paralysis and pain. Not surprising, all forms of distress were strongly associated with long-term psychological consequences, such as flashbacks, insomnia, fear of future surgery, and PTSD.
Psychophysiological mechanisms of PTSD
The alert, non-stressed brain benefits from a top–down management system, such that the medial prefrontal cortex (mPFC) down-regulates amygdala-driven fear conditioning
stressed brain is marked by a diminished capacity of the mPFC and the hippocampus to act as checkpoints on the excitatory flow that emerges from the amygdala
mportance of the inhibitory control of the mPFC over the amygdala
Inhibition of long-term potentiation of the γ-aminobutyric acid type A receptor in the hippocampus
and other parts of the medial temporal lobe memory system – amygdala and the hippocampal region including perirhinal, entorhinal, and parahippocampal cortices –
are associated with amnesia during anaesthesia
downregulate glutamatergic and norepinephrine pathways emanating from the amygdala
ainful stimuli may further increase amygdala activity. +
Hence, the amygdalar activity surge during AAGA may lay down a permanent emotionally traumatic memory (PTSD) through excitotoxic long-term potentiation
Psychological assessment and diagnosis
f panic, extreme fear, dissociation, suffocation, and fear of dying. In some, the distress persisted with long-term symptoms of post-traumatic stress. The distress of AAGA may emerge soon after the event, qualifying it as an acute stress disorder (ASD).
9 symptoms or more from the five categories of
intrusion,
negative mood,
dissociation,
avoidance, and
arousal is
required to make the diagnosis of ASD,
ASD ranges between 3 days and 1 month after exposure to the traumatic event
irritable behaviour, and angry outbursts
Sleep disturbance
Post-traumatic stress disorder is diagnosed when these symptoms last for more than 1 month after a traumatic event. Some patients do not initially present with PTSD, making the diagnosis challenging
h upsetting memories, nightmares, flashbacks, distress after traumatic reminders, and physical reactivity after exposure to trauma reminders.
(Psych SOS)
AAGA substantially increased the risk of PTSD.
Risk Factors for post-surgical PTSD
poor social support;
history of PTSD;
prior mental health treatment;
dissociation related to the surgery;
perceiving that one’s life was in danger during surgery; and
intraoperative awareness.
Management
Pharm
To our knowledge, there are no specific treatment guidelines for AAGA.
extrapolated from our current understanding of general PTSD.
no evidence-based psychopharmacological recommendation that prevents ASD and PTSD in patients at risk
selective serotonin reuptake inhibitors (SSRIs) can be used for both ASD and PTSD. SSRIs are recommended as first-line medication for PTSD because they can reduce symptoms of re-experiencing, avoidance, numbing, and hyperarousal
SSRIs are also effective for psychiatric disorders that frequently coexist with PTSD (e.g. depression, panic disorder, social phobia, and obsessive-compulsive disorder).
Benzodiazepines may reduce acute anxiety and help with sleep, but they have not been establised to prevent ASD or PTSD, or treat the core symptoms of PTSD.
Benzodiazepines may reduce acute anxiety and help with sleep, but they have not been establised to prevent ASD or PTSD, or treat the core symptoms of PTSD.
Management
Early supportive psychotherapeutic interventions,
along with psychoeducation and
case management that encourage reliance on
inherent resilience and
good sound judgement,
can be very beneficial after acute trauma.
This is because they promote engagement in ongoing care
may also benefit from cognitive behavioural therapy with an exposure component.
Eye movement desensitisation and reprocessing, which includes a brief, interrupted exposure-based therapy, directed eye movements, along with recall and venting of traumatic memories in the setting of relaxation response elicitation, may also be helpful
Stress inoculation, imagery rehearsal, and prolonged exposure techniques may reduce PTSD-associated anxiety and avoidance symptoms.
Desipramine, fluoxetine, paroxetine, phenelzine, risperidone, sertraline, and venlafaxine were more effective than placebo for symptomatic PTSD
hus, evidence supports a choice of psychotherapeutic approaches as first-line treatments for PTSD. It is notable that treatment combining both psychotherapy and psychopharmacology was superior in the long term.
The NAP5 awareness support pathway emphasises the importance of:
(i) face-to-face postoperative meeting with patients that experience AAGA;
(ii) early consultation with a psychiatrist or
psychologist and
early assessment of flashbacks,
nightmares, new level of anxiety,
and depressed mood; and
(iii) active follow-up at 2 weeks to assess
for new or ongoing needs for treatment referrals.
Q3 — NAP6 report on anaphylaxis
a) List the four common triggers for perioperative anaphylaxis
according to the report of the National Audit Project 6 (NAP6)
from the Royal College of Anaesthetists.
● Antibiotics — 44%.
● Muscle relaxants — 33%.
● Chlorhexidine — 9%.
● Patent blue dye (used in breast surgeries) — 5%.**
b) What is the estimated incidence of perioperative anaphylaxis?
One in 10,000.
c) Outline the pathophysiological process of anaphylaxis.
● Immunologically-mediated response.
● The suspected antigen combines with immunoglobulins (IgE) causing mast cell degranulation
with the release of vasoactive mediators
(e.g. histamine, tryptase, leukotrienes, prostaglandins, etc.)
with its effects on various systems.
● Cardiovascular system —
intravascular volume redistribution causing reduced blood pressure associated with
reduced cardiac output and reduced coronary perfusion.
● Capillary leak —
causing angioedema,
laryngeal oedema, urticaria
and hypotension.
● Smooth muscle contraction in the
respiratory system and abdomen
leading to bronchospasm and
abdominal pain/cramps, respectively
d) Describe your management of intraoperative anaphylaxis in an adult patient.
● Recognition of anaphylaxis from other differential diagnoses.
● Remove the trigger for anaphylaxis.
● Call for help.
● ABCDE approach,
monitoring of oxygen saturation, ECG and noninvasive
blood pressure as the minimum requirement.
● Treat life-threatening problems first,
e.g. if blood pressure is <50mmHg or cardiac arrest —
CPR in accordance with the ALS®
algorithm,
immediate adrenaline and IV crystalloid boluses.
● The drug of choice is adrenaline —
dose 500μg IM (1:1000) or
50μg boluses IV (1:10000) (boluses as needed).
● Consider an adrenaline infusion if needed —
administer in monitored settings.
● For refractory hypotension —
consider a vasopressin 2 IU bolus and repeat as necessary.
● IV crystalloid fluid boluses — 20ml/kg bolus as needed.
● Second-line drugs —
chlorphenamine 10mg IM or a slow IV in adults;
hydrocortisone — 200mg IV in adults.
● Serum mast cell tryptase levels —
as soon as possible after emergency treatment,
1-2 hours later and 24 hours later
(as a baseline).
● Other steps in management:
- 100% oxygen;
- if there are circulation problems —
flatten the operating table with the legs up; - if there are airway and breathing problems —
early tracheal intubation in airway obstruction;
head up (propped up position) to facilitate ventilation; - if the patient has stridor —
use an adrenaline nebuliser (400μg/kg); - watch for the biphasic response of anaphylaxis;
- observation for 12-24 hours —
consider transfer to the ITU if needed; - appropriate documentation in the notes.
e) What should be done after successful treatment of
anaphylaxis?
● Referral to an allergy specialist.
● Communication with the patient and family regarding the events and
actions taken must be done by the anaesthetists as well as allergy
doctors.
● Anaphylaxis education for patients — avoidance of the allergen.
A healthy 39-year-old male is anaesthetised with a general anaesthetic for a laparoscopic cholecystectomy. As soon as the skin incision is made, it is noted that the core temperature is rising quickly. This is associated with a rise in etCO2 and an increase in heart rate.
a) What are the differential diagnoses in this condition?
● Malignant hyperthermia.
● Mechanical causes:
- inadequate FiO2;
- inadequate ventilation;
- problems with the anaesthetic machine or breathing circuit.
● Surgical:
- laparoscopy with gas insufflation;
- tourniquet ischaemia;
- endocrine emergencies.
● Anaesthetic:
- inadequate analgesia;
- anaphylaxis;
- cerebrovascular event.
● Patient-related:
- anaphylaxis;
- sepsis;
- neuromuscular disorders;
- phaeochromocytoma.
● Others — serotonin syndrome.
b) What is malignant hyperthermia?
A progressive,
life-threatening hyperthermic reaction
occurring during general anaesthesia.
c) Name some triggers for malignant hyperthermia.
● Neuromuscular blockers — suxamethonium.
● Volatile agents — halothane, enflurane, isoflurane, desflurane,
sevoflurane.
d) What is the pathophysiology of malignant hyperthermia?
● Exposure of the trigger causes dysregulation of excitation —
contraction coupling (EC) in the skeletal muscle.
● Changes in ryanodine receptor (RyR) isoforms and dihydropyridine receptors (DHPRs).
● Sustained release of calcium into cytosol.
● Increased metabolic demand for ATP causes an increase in CO2 production and O2 consumption.
● A rise in CO2 stimulates the sympathetic system and the heart rate increases.
● Muscle contraction causes acceleration of heat production and
muscle rigidity progresses.
e) How would you manage malignant hyperthermia?
● Early diagnosis is the key.
● Get more help.
● Stop the volatile agent,
use 100% oxygen, hyperventilate, eliminate all
triggers.
● Use activated charcoal filters in the circuit (
volatile-free machine).
● Intravenous anaesthesia.
● Dantrolene — start at 2.5mg/kg
(mixing in 60ml for each vial is time
consuming, and so ask for help by
assigning one other person the
responsibility to prepare this).
● Further doses of 1mg/kg dantrolene.
● A reaction can recur after up to 14 hours of resolution.
● Switch off warming devices.
● Active cooling measures.
● Blood samples, bladder catheter, CVP catheter.
● Treat hyperkalaemia with dextrose insulin or calcium chloride or haemofiltration (especially in rhabdomyolysis).
● Correct acidosis.
● Treat arrhythmias if any.
● Treat acute kidney injury — diuresis, alkalinise the urine.
● Treat coagulopathy.
● Monitor in intensive care unit
f) How would you confirm the diagnosis of malignant
hyperpyrexia?
● In vitro contracture testing with a muscle biopsy
(European MH group guidelines, 2015).
● DNA sequencing technology.
BJA Key pts
*
Enquiry about a family history of problems with anaesthesia is a mandatory part of the anaesthetic history.
*
Wherever possible, a patient suspected of being at risk of MH should have their status verified with confirmatory tests.
*
Conditions associated with variants in the RYR1 gene may also carry a risk of malignant hyperthermia.
*
Suxamethonium and potent inhalational anaesthetics are contraindicated in patients susceptible to MH.
*
Activated charcoal filters enable rapid preparation of the anaesthesia workstation for patients susceptible to MH.
BJA MH
Malignant hyperthermia (MH) is a potentially lethal reaction to drugs used during general anaesthesia that occurs in genetically predisposed individuals
Another key element in reducing mortality and morbidity from MH is the identification of individuals who are genetically predisposed to develop MH (MH-susceptible) before anaesthesia so that they are not exposed to MH-triggering drugs.
n. Estimates based on clinical epidemiological data suggest a prevalence of up to 1:10,000, but those based on the prevalence in large genomic databases of genetic variants known to be associated with MH suggest that 1:1500 people may be MH-susceptible
MH-susceptible patients may have had several uneventful anaesthetics, which is why a family history of anaesthetic problems is a mandatory part of the anaesthetic history.
The Department of Anaesthesia at CUH, incorporating Intensive Care and Pain Medicine also provides support for patients with Malignant Hyperthermia (MH) and their families, and for clinicians caring for a patient with MH.
Dr. Peter Lee, Consultant Anaesthetist, is the lead in this area.
DX
Diagnosis of MH susceptibility can be confirmed either through genetic testing or a muscle biopsy with in vitro contracture tests (IVCT) of the excised musc
If confirmation of the diagnosis is not in the patient’s medical records, the patient may carry correspondence or warning cards/tags issued by the diagnostic service that provided their diagnosis.
FH
amily have been tested and found susceptible to MH. We strongly recommend that the relevant diagnostic MH unit is contacted in order to verify the history.
if a relative between the family index case and the current patient has been shown not to be susceptible, the patient is not at risk
Conditions associated with an increased risk of MH
1 Congenital myopathy
Only myopathies with an RYR1 or STAC3 genetic aetiology are implicated
- Exertional rhabdomyolysis
Some causes of rhabdomyolysis are known not to be associated with MH (e.g. CPT2 deficiency, McArdle disease) - Exertional heat illness
Exclude extrinsic factors (e.g. drugs, concurrent illness, extreme environments) - Idiopathic hyperCKaemia
Possible association with MH is a diagnosis of exclusion of other causes - Carrier of RYR1 variant of unknown significance Nonsense variants leading to a loss of function in the protein are not implicated in MH
Perioperative management of patients with suspected MH susceptibility for elective procedures
If diagnosis established—proceed with trigger-free anaesthesia.
If diagnosis not established—consider the risk of proceeding with trigger-free anaesthesia or postponing the procedure until a diagnosis may be established.
The European Malignant Hyperthermia Group has recently published guideline recommendations for management of anaesthesia for a patient who is MH-susceptible