NICE pre-operative guidelines: Summarise NICE guidelines on pre-operative investigations.
All types of surgery:
ASA Grades
Minor Surgery
Intermediate surgery
Major Complex Surgery
Peri-operative risk scoring systems: summarise common peri-operative risk scoring systems (ASA and POSSUM).
ASA Grades
POSSUM - score of 1,2,4,8
Peri-operative disease management: explain the principles of perioperative management of medical co-morbidities, including diabetes mellitus, hypertension, ischaemic heart disease, asthma, COPD, patients on anti-coagulant medications and sickle cell disease.
Minor Surgery
Intermediate surgery
Major Complex Surgery
Day Surgery: recall the criteria for the suitability of patients for day stay surgery.
Safety - Nil by mouth policy: explain the principles of nil by mouth policy before surgery.
Preoperative fasting is the practice of a patient abstaining from oral food and fluid intake for a time before an operation is performed. This is intended to prevent pulmonary aspiration of stomach contents during general anesthesia.
The amount of time you have to go without food or drink (fast) before you have your operation will depend on the type of operation you’re having. However, it is usually at least 6 hours for food, and 2 hours for fluids. You’ll be told how long you must not eat or drink for before your operation.
Safety - Transfusion reporting - recognize the importance of reporting blood units administered to the transfusion lab.
Ensuring that incidents are reported through the Trust Incident Reporting procedure, in line with the Incident Reporting and investigation Policy, and ensuring there is resultant organisational learning through the divisional structure and more widely across the trust.
Reporting of transfusion reactions or other incidents to the Blood Transfusion Laboratory.
Any unexpected event that has an actual or potential short-term or long-term detrimental effect on a patient must be reported according to the Trust’s Incident Reporting and Investigation Policy and to the Blood Transfusion laboratory.
Incident reporting should include ‘near miss’ episodes involving procedural errors which were detected in time to prevent a serious complication of blood transfusion, for example taking the blood sample for compatibility testing from the wrong patient or labeling the blood sample with another patient’s details.
Safety - controlled drugs: recognize the importance of recording the use of controlled drugs in the controlled drug register.
Respiratory - Ventilation: compare the differences between spontaneous ventilation and positive pressure ventilation.
Spontaneous breathing - the movement of gas in and out of the lungs that is produced in response to an individual’s respiratory muscles.
Continuous spontaneous ventilation - any mode of mechanical ventilation where every breath is spontaneous (e.g. patient triggered and patient cycled)
Positive pressure ventilation - a form of respiratory therapy that involves the delivery of air or a mixture of oxygen combined with other gases by positive pressure into the lungs.
Delivered in 2 forms:
BiPAP - Bi-level Positive Airway Pressure
- 2 levels of pressure - inspiratory positive airway pressure (IPAP) and lower expiratory positive airway pressure (EPAP) for easier exhalation
CPAP - Continuous Positive Airway Pressure
APRV - Airway Pressure Release Ventilation
Respiratory - Anaesthetic emergencies: recall the assessment and management of anaesthetic emergencies, including asthma, pneumothorax, haemothorax, anaphylaxis, foreign body aspiration.
ASTHMA
Assessment:
While recognizing the poor correlation between clinical signs and physiological measures, an FEV1 of <30% predicted is likely to be present in a patient who is unable to speak more than a few words with an arterial carbon dioxide tension (PaCO2) of >5.3 kPa (40 mm Hg), a quiet chest with the absence of audible wheezing, respiratory rate >30/min or pulsus paradoxus >20 mm Hg.
Management - OSHITME
O - OXYGEN - give via nasal cannula / mask to get O2 sats between 94-985
S - SALBUTAMOL - 2.5-5mg nebulised
H - HYDROCORTISONE - 100mg IV or PREDNISOLONE 40mg oral
I - IPRATROPIUM - 500mcg nebulised
T - THEOPHYLLINE - IV
M - MAGNESIUM SULPHATE - IV
E - ESCALATE CARE - if intubation and invasive ventilation are required
The administration of excessive oxygen is not without potential risks, including atelectasis and increased intrapulmonary shunting, and a reduction in cardiac output and coronary blood flow
NIPPV - useful for those with hypercapnic respiratory failure, as long as airway protection & can tolerate face mask. Will reduce work of breathing, respiratory muscle fatigue, decrease airway resistance, re-expand atelectatic areas of lung, decrease adverse hemodynamic effects of negative inspiratory pleural pressures - buying time for transfer to an ICU / HDU and for pharmacological intervention to take effect.
https://thorax.bmj.com/content/62/5/447
PNEUMOTHORAX & HAEMOTHORAX
Assessment
Management
- Perform decompression before imaging only if they have either haemodynamic instability of severe respiratory compromise
ANAPHYLAXIS
Pathway:
FOREIGN BODY INSPIRATION
Presentation:
Management:
Respiratory - Observations: recall the measurement and normal values of physiological parameters, including pulse oximetry, capnography and blood gas results.
Pulse Oximetry
Capnography
Blood Gas Results
Circulation - Blood pressure monitoring: recall the indications for non-invasive and invasive monitoring.
Invasive:
Non-invasive:
- Patients who are at risk of haemodynamic instability
Circulation - IV fluids: explain the rationale of fluid administration and the difference between colloids and crystalloids.
Colloids
Crystalloids
Adults (>16) - 1 unit of plasma to 1 unit of red blood cells to replace fluid volume
Children (<16) - 1 part plasma to 1 part red blood cells and base volume on child’s weight.
Circulation - Blood transfusion: recall the triggers for giving a blood transfusion.
Pain relief - Multi-modal analgesia: recall the principles of multimodal analgesia.
Combination of regional anaesthesia (single-shot or continuous central neuraxial or peripheral nerve blocks or local infiltration analgesia), opioid analgesics and non-opioid systemic analgesics (paracetamol, NSAIDs).
Pain relief - Pain: summarise approaches to the management of acute and chronic pain.
https://midessexccg.nhs.uk/about-us/the-library/medicines-management/clinical-pathways-and-medication-guidelines-1/chapter-4-central-nervous-system-2/3345-acute-and-chronic-combined-pain-guidelines-august-2019/file
Pain relief - WHO pain ladder: explain the WHO pain ladder.
Mild pain
- Non-opioid + adjuvant therapy
Mild to Moderate pain
- Weak opioid or multimodal + non-opioid + adjuvant therapy
Moderate to Severe Pain
- Strong opioid + non-opioid + adjuvant therapy
Severe to Very Severe Pain
- Interventional treatments + non-opioid + adjuvant therapy
Pain relief - Regional analgesia/anaesthesia: explain the rationale and management of regional analgesia/anaesthesia
Regional anaesthesia may be classified anatomically as follows: (a) infiltration anaesthesia (extravascular or intravascular); (b) peripheral nerve blockade (minor or major nerve block); and (c) central neural blockade (epidural or subarachnoid block).
The local anaesthetic agents commonly employed for regional anaesthesia may be classified according to their relative potency and duration of activity into: (1) agents of low potency and short duration, e.g. procaine and chloroprocaine; (2) agents of moderate potency and duration, e.g. lignocaine (lidocaine), mepivacaine and prilocaine; and (3) agents of high potency and long duration, e.g. amethocaine (tetracaine), bupivacaine and etidocaine.
In general, the onset, duration and quality of regional anaesthesia are enhanced by an increase in dose achieved by either an increase in concentration or in the volume of anaesthetic solution, and by the concomitant use of a vasoconstrictor drug, adrenaline (epinephrine). However, the local anaesthetic properties of the intrinsically more potent and longer acting agents are influenced less by the addition of adrenaline, particularly when such agents are employed for central neural blockade of the epidural type.
Pain relief - Analgesic Drugs: recall dosage, mode of administration, indications and contraindications of common analgesic drugs.
NON-OPIOIDS
Paracetamol
Aspirin
Indications: Headache, transient MSK pain, dysmenorrhoea, pyrexia, anti-platelet
Contraindications: Gastric irritation (can se enteric coated preparations), warfarin sodium interaction
Other NSAIDS
OPIOIDS + NON-OPIOIDS
ADDITION OF CAFFEINE
MORPHINE
BUPRENORPHINE
DIAMORPHINE HYDROCHLORIDE (Heroin!)
ALFENTANIL, FENTANYL, REMIFENTANIL
METHADONE HYDROCHLORIDE
OXYCODONE HYDROCHLORIDE
PENTAZOCINE
PETHIDINE HYDROCHLODIRDE
TAPENTADOL
TRAMADOL HYDROCHLORIDE
CODEINE PHOSPHATE
- Relief of mild to moderate pain where other painkillers such as paracetamol or ibuprofen have proved ineffective
DIHYDROCODEINE TARTRATE
MEPTAZINOL
NB: Post-operatively - morphine most widely used.
Pain relief - Anti-emetic drugs: recall dosage, mode of administration, indications and contraindications of common anti-emetic drugs.
ANTIHISTAMINES - e.g. promethazine
- Vomiting during pregnancy
PHENOTHIAZINES
HALOPERIDOL & LEVOMEPROMAZINE
- In terminal illness - antipsychotic drugs
METOCLOPRAMIDE HYDROCHLORIDE
DOMPERIDONE
GRANISETRON & ONDANSETRON
- In patients receiving cytotoxics and post-operative N&V
PALONOSETRON
DEXAMETHASONE
APREPITANT & FOSAPREPITANT & ROLAPITANT
NABILONE
PREGNANCY
POST-OP
MOTION SICKNESS
NB: Domperidone, metochlopramide hydrochloride, 5HT3-receptor antagonists, phenothiazines ineffective in motion sickness.
VESTIBULAR DISORDERS
Temperature control - Homeostasis: recall the normal homeostatic control of temperature and explain how this is affected by anesthesia.
Perioperative hypothermia develops in three distinct phases:
(1) anaesthetic-induced vasodilation during induction of anaesthesia results in core-to-peripheral redistribution of body heat and decreases core temperature 1–1.5°C during the first hour of general anaesthesia
(2) subsequently core temperature decreases linearly as heat loss to the environment exceeds metabolic heat production
(3) after 3–5 h of anaesthesia, core temperature often stops decreasing.
This core temperature plateau results from reactivation of thermoregulatory vasoconstriction which decreases cutaneous heat loss and constrains metabolic heat to the core thermal compartment.
Perioperative hypothermia is associated with numerous complications such as myocardial ischaemia, increased risk of wound infection and coagulopathy. On the other hand temperatures only 1–3°C below normal provide substantial protection against cerebral ischaemia and hypoxaemia in numerous animal species. Consequently, most anaesthesiologists believe mild hypothermia is indicated during operations likely to cause cerebral ischaemia such as carotid endarterectomy and neurosurgery or cardiac procedures.
Temperature control - Warming devices: recall methods of warming patients during surgery, including warm air blanket, fluid warmers and heat moisture exchangers.
WARM AIR BLANKET
Filters air and then forces warm air through a disposable blanket which covers the patient before, during and after surgery
FLUID WARMERS
A medical device used in healthcare facilities for warming fluids, crystalloid, colloid, or blood product, prior to being administered (intravenously or by other parenteral routes) to body temperature levels in order to prevent hypothermia in physically traumatized or surgical patients.
HEAT AND MOISTURE EXCHANGER
Devices used in mechanically ventilated patients intended to help prevent complications due to drying of the respiratory mucosa, such as mucus plugging and endotracheal tube (ETT) occlusion.
Emergence: recognise the requirements for emergence from anaesthesia and the indications for ongoing sedations.
Receptors:
Functionally, the drug-receptor interaction leads to several changes in cortical and subcortical signals, inducing alterations in the connectivity across brain regions. Complex mechanisms underlie alterations of cortico-cortical and cortical-subcortical functional connectivity. The different general anesthetics activate different molecular patterns, expressed as different functional alterations in brain connectivity and different electrophysiological correlates.
Volatile agents, for instance, interfere with frontal-posterior connectivity and this effect reverberates on the gamma (20–60 Hz) oscillations which have a pivotal role in arousal and maintenance of consciousness.
Again, propofol provokes a quick anteriorization of alpha rhythms (8–12 Hz) and promotes the propagations of slow-delta oscillations across the cortex, inducing a functional disruption of the connectivity between distinct cortical areas.
Yet, dexmedetomidine impairs the thalamo-cortical functional connectivity mostly expressed as spindle waves (12–16 Hz) in the frontal area.9 The matter is extremely complex, as alterations in connectivity within distinct brain regions lead to different depths of anesthesia.
Thus, changes in thalamic-cortical connectivity lead to the induction of the loss of consciousness (LoC) whereas changes in the cortico-cortical functional connectivity and a further impact on cortico-subcortical functioning induce the completion of the induction mechanism and the maintaining of the surgical anesthesia status.
During the AE phase, mechanisms responsible for LoC and anesthesia maintenance are gradually reversed. Nevertheless, these “passive” processes are associated with specific awakening mechanisms.
Of note, these active processes include several ascending arousal brain pathways where the thalamus plays a key role.
Apart from the thalamus, other arousal-promoting brain regions such as the substantia nigra, the ventral and laterodorsal tegmental areas of the midbrain, the dorsal raphe, and the locus ceruleus (LC) as well as the basal forebrain (BF), and lateral hypothalamus are involved. Thus, it has been postulated the existence of a mesencephalic arousal pathway.
The hypothalamus is also implicated in these wake-promoting processes. Orexin also known as hypocretin, is an endogenous wakefulness-promoting substance.
Hypothalamic orexinergic neurons are involved in both the sleep-to-wake transition and maintenance of wakefulness.
This orexinergic system is functionally connected with other structures such as basal ganglia that regulate the awakening processes during the AE. Interestingly, serotonergic neurons in the dorsal raphe nucleus receive projections from orexinergic neurons, concurring in sleep-wakefulness modulation.
Among these complex arousal networks, there are the LC norepinephrine (LCNE) system and posterior hypothalamic histaminergic tuberomammillary nuclei (TMN). In particular, the LCNE is the main structure of the so-called LCNE arousal system which includes the posterior cingulate cortex, thalamus, and basal ganglia. Another arousal pathway is the brainstem ascending reticular arousal system (ventral and dorsal pathways) which originates from the pontine/midbrain regions and develops cholinergic cortical projections through interactions with the thalamus, hypothalamus, and the BF region.
In summary:
i) AE is not just a passive process due to a cessation of the action of general anesthetics
ii) the arousal mechanisms at the end of GA are produced by structures deeper in the brain, rather than being activated within the neocortex
iii) rather than a single awakening system, it is more correct to refer to an arousal network. It is composed by the cholinergic basal forebrain, dopaminergic ventral tegmental area, anterior cingulate cortex, orexinergic hypothalamic, serotonergic raphe, LCNE, and histaminergic TMN neurons.
Recovery - Observations: recall the observations measured in recovery.
Physical assessment:
Recovery - Discharge: recall the criteria for discharge from recovery.
PACU Discharge Criteria: