2018 Feb FRCA Flashcards
1.1 Define Sedation
Sedation, also known as “monitored anesthesia care”,
is a continuum
ranging from minimally impaired conciouesness to unconciousness
Medications are given,
usually through an IV,
to make the patient feel drowsy and relaxed.
Different levels of sedation are possible, depending on the type of procedure and the patient’s preference.
1.2 What are the ASA Classifications of Sedation?
- Minimal Sedation
Anxiolysis - Moderate Sedation/Analgesia
(“Conscious Sedation”) - Deep Sedation/
Analgesia - General Anesthesia
What are the clinical criteria at each level?
- Responsiveness
- Airway
- Spontaneous Ventilation
- Cardiovascular Function
Responsiveness
- Normal response to verbal stimulation
- Purposeful** response
to verbal or tactile
stimulation - Purposeful** response
following repeated
or painful stimulation - Unarousable even
with painful stimulus
Airway
Unaffected
No intervention required
Intervention may be required
Intervention often require
Spontaneous Ventilation
Unaffected
Adequate
May be inadequate
Frequently inadequate
Cardiovascular
Function
Unaffected
Usually maintained
Usually maintained
May be impaired
1.4 Dissociative Sedation
Trancelike
cataleptic state
profound analgesia and amnesia
Maintaining protective airway reflex
spontaneous resp
CV stability
Between moderate and deep
1.5.a
What is the mechanism of action of midazolam?
Midazolam is a γ-aminobutyric acid A (GABAA) receptor agonist
This results in the sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties for which the drugs are prescribed.
1.5.b What is it’s time to peak onset
and elimination half life
IV Onset ~2 min
Maximum effect is in about 5 to 10 minutes.
The elimination half-life of midazolam is between 1.5 - 2.5 hours
What adverse errors can occur with sedation and causes of same
Dose
Inappropriate dose given - causing over sedation
Respiratory compromise
Certain agents - ie midazolam can affect respiratory effort - in extreme may require advanced resp support
HD compromise
Propofol can lead to decrease in CO / drop in SVR - may cause hypotension
Aspiration
Deeply sedated patient may lose protective airway reflexes and are at risk of aspiration of gastric contents
Delirium
Increased risk of delirium in older age group
Agitation / hyperactivity
Midazolam can cause a paradoxical hyperactivity in some patients
2.1 Define counter -pulsation
Counter-pulsation is a term that describes
balloon inflation in diastole
and deflation in early systole.
2.2 Physiological mechanism of IABPs
Inflation: >> Forces blood proximally, increasing the pressure within the proximal aorta compared to the left ventricle, thus improving perfusion of coronary arteries, increasing oxygen delivery.
> > Forces blood distally,
thus augmenting the apparent
output from the left ventricle.
> > Augments Windkessel effect.
Deflation:
» Decrease in afterload reduces myocardial wall stress during systole, thus
reducing myocardial oxygen demand.
2.3 Indications for IABP
Indications:
» Cardiogenic shock due to myocardial infarction if revascularisation planned.
> > Acute mitral regurgitation or ventricular septal defect due to acute myocardial infarction.
> > Refractory ventricular arrhythmias whilst awaiting definitive treatment.
> > Refractory unstable angina if treatment option available.
> > Refractory left ventricular failure if destination treatment planned.
> > Perioperative support for high-risk coronary artery bypass surgery.
> > Perioperative support for high-risk non-cardiac surgery
2.3 ContraIndications IABP
Contraindications:
Absolute
» Aortic regurgitation, dissection or stent.
> > Chronic end-stage heart disease with no further possible intervention.
Relative
> > Uncontrolled sepsis.
> > Abdominal aortic aneurysm, severe peripheral vascular disease or arterial reconstruction surgery.
> > Uncontrolled bleeding disorder.
> > Tachyarrhythmias.
2.4 List the possible complications
of an IABP. (6 marks)
> > Haemodynamic compromise due to poor timing of counter pulsation or malposition.
> > Limb, spinal cord or visceral (especially renal) ischaemia.
> > Compartment syndrome.
> > Aortic dissection.
> > Vascular injury causing bleeding, haematoma, false
aneurysm, arteriovenous fistula.
> > Cardiac tamponade.
> > Thromboembolism.
> > Thrombocytopaenia and haemolysis.
> > Infection.
> > Balloon rupture resulting in gas embolus.
3.1 Abdominal Compartment Syndrome
Define Intra Abdominal Hypertension
Intra-abdominal hypertension is a sustained or repeated IAP > than 12 mmHg
Define Abdominal Compartment Syndrome
Abdominal compartment syndrome is defined
as a sustained IAP greater than 20 mmHg
with a new organ dysfunction or
failure regardless of
abdominal perfusion pressure (APP)
3.3 Systemic effects of Abdominal Compartment Syndrome
CVS
Resp
Systemic effects of intra-abdominal hypertension
Cardiovascular effects of increased intra-abdominal pressure
1 Reduced venous return
2 Reduced cardiac output
3 Increased systemic vascular resistance
Pulmonary effects of increased intra-abdominal pressure:
1 Reduced PaO2/FiO2 ratio
2 Hypercarbia
3 Increased inspiratory pressure
3.3 Systemic effects of Abdominal Compartment Syndrome
Renal
CNS
GI
Renal effects of increased intra-abdominal pressure
1 Reduced glomerular filtration
2 Oliguria
CNS
Acute elevations of IAP may also increase intracranial pressure.
Gastrointestinal effects
Gut mucosal ischaemia, independent of changes in cardiac output,
occurs with an increase in IAP
3.3 - Pathphpysiology of AC
Pathophysiology
Chronic increase in intra-abdominal volume
can be compensated by changes
in the abdominal wall compliance.
In situations where the volume of the
abdominal contents increases rapidly or the
abdominal wall compliance reduces,
IAP increases.
Initially, the abdominal wall distends but, eventually,
a critical volume is reached and the compartment syndrome occurs.
Factors such as the rapidity of the increase and the presence of muscle spasm secondary to peritonism can affect the critical volume.
A rapid increase in the volume of the
abdominal contents occurs in many situations such
as haemorrhage or blunt abdominal trauma.
Also, capillary leak, interstitial oedema and disseminated intravascular coagulation may result in ascites, ileus and bowel wall oedema.
Gas, whether inside or outside the bowel, faeces and foreign bodies, e.g
. surgical packs, can all contribute to the
increase in pressure.
3.4
Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
Anaesthetic management for abdominal decompression
1 Severe instability may preclude the transport of the patient to the operating theatre.
2 Although concerns have been raised about the potential difficulty of managing haemorrhagic complications,
many centres now routinely perform decompression within the Intensive Care Unit.
3 The pharmacokinetics and pharmacodynamics of anaesthetic agents may be altered in the presence of intra-abdominal hypertension.
4 Patients with ACS may be more sensitive to the cardio- vascular depressant effects of anaesthetic agents; changes in organ blood flow and altered volumes of distribution may increase their potency
3.4 Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
The abdominal decompression syndrome
During abdominal decompression, three potentially dangerous physiological changes occur.
- A sudden drop in systemic vascular resistance
Although the use of epinephrine has been advocated inthis situation, most centres use an approach of aggressive preloading with fluids.
- A fall in intrathoracic pressure Many patients with ACS require ventilatory pressures of
approximately 50 cm H 2 O together with high levels of
PEEP.
Sudden decreases in intrathoracic pressure may
result in the administration of inappropriately large tidal
volumes and alveolar over-distension, producing both
barotrauma and volutrauma.
3 The washout of toxic products
Ischaemic metabolism causes accumulation of lactic acid, adenosine and potassium within the tissues. Following the restoration of circulation, these products rapidly return to the general circulation producing arrhythmia, myocardial depression and vasodilatation.
Asystolic cardiac arrest has been reported in up to 25% of patients undergoing decompressive laparotomy and is reported as being universally fatal.
The decompression syndrome may be ameliorated by the prior administration of a ‘reperfusion cocktail’.
This consists of 2l of 0.45% normal saline containing 50 g of mannitol and 50 milliequivalents of sodium bicarbonate.
3.4 Anaesthetic considerations for patient coming to theatre for treatment of
Abdominal Compartment Syndrome
Management after decompression
Closure of abdomen after decompression may not be possible for several days because of bowel oedema.
Fluid requirements in a patient with an open abdomen are massively increased (up to 10–20 l day1 ).
Hypothermia remains a risk and core temperature monitoring is required.
Despite decompression, ACS may recur.
Therefore, intravesical pressure monitoring should continue after decompression.
Enteral feeding is well tolerated by patients with an open abdomen and may speed the resolution of gut oedema.
Reperfusion injury to the gut and kidneys may also occur after delayed decompression with subsequent development of multi-organ dysfunction
4.1 3 Chemicals in Cigarettes
- Nicotine
- Carbon Monoxide
- Arsenic
- Ammonia
- Methanol
4.2 a Cardiovascular system effects of cigarette smoking
Cardiovascular
- Hypertension Peri-operative ischaemia
- Ischaemic heart disease Myocardial infarction
- Hypercoagulation Thrombosis
Worst outcome after coronary artery bypass graft surgery and vascular
surgery
Smokers are prone to hypertension, ischaemic heart disease, cerebrovascular disease and heart failure.
All of these are risk factors for postoperative cardiovascular morbidity and mortality.
Smokers also have higher resting plasma catecholamine concentrations than
non-smokers and an exaggerated sympathetic response to desflurane anaesthesia.
The electrocardiograms of smokers are more
likely to show ST segment depression during general anaesthesia, implying impaired coronary perfusion that, together with hypoxaemic effects of COHb,
reduces myocardial O2 supply during the
peri-operative period, especially when the demand is increased.
This phenomenon is reflected in the reduced time of onset of exercise-induced angina and the increased incidence of ventricular dysrhythmia and dysfunction in the awake subject with COHb values
of as little as 4.5–6%.
Myocardial ischaemia itself promotes carboxymyoglobin formation reducing myocardial O2
supply still further,
which, together with the effect of CO on cytochrome oxidase
may explain the known negative inotropic effect of CO.
4.2 b Respiratory system effects of cigarette smoking
Respiratory
Decreased oxygen carriage
Hypoxaemia
Irritable upper airways
Laryngospasm
Irritable lower airways
Bronchospasm
Depressed ciliary function
Retained secretions and
infection
Decreased FEV 1
Increased closing capacity
4.2 b - O2 Carriage detail
Oxygen carriage in blood
Oxygen and haemoglobin (Hb) interact in a characteristic fashion to give the well-known
oxygen–haemoglobin dissociation curve.
Under normal circumstances, after blood has passed
through the lungs, Hb is almost fully saturated
with O2 even when the concentration of O2
in the lungs (and, therefore, in arterial blood) is slightly
reduced.
In tissues, where pH is lower and CO2
concentration and temperature are greater, the
characteristics of Hb favour O2 release.
In smokers, several changes occur. Blood con-
centration of carbon monoxide (CO) is increased
to as much as 10% (normal 2%). This has two
effects on O2 carriage.
First, Hb has 250 times more affinity for
CO than for O2, so the total amount of Hb available for O2 carriage is markedly decreased.
Secondly, CO shifts the dissociation
curve to the left, which reduces the ability of Hb to release O2.
To make matters worse, CO also inhibits cytochrome oxidase, the enzyme that is needed for the final oxygen dependent synthesis of ATP in the mitochondria.
This compromise of O2 delivery
makes the events that ordinarily tend to reduce O
2 saturation (i.e. induction of anaesthesia, intra- and peri-operative critical incidents, postoperative hypoventilation and atelectasis)
more threatening for smokers.
With values of carboxyhaemoglobin (COHb)
approaching 10–15%, the smoker may already be near the point on the dissociation curve where any further reduction in PaO2 will lead to rapid desaturation.
The light absorbance of COHb is nearly the same as that of oxygenated Hb at the wavelengths used by bedside pulse oximeters.
Thus, they cannot differentiate COHb from oxyhaemoglobin and over-estimate O 2
saturation.
Just as reliance on oximeters in othersituations of severe CO excess (e.g. house fires) is dangerous, an
apparently normal reading can lead to a false sense of security in heavy smokers
4.2 b Airways
Smokers have ‘irritable’ upper airways and this increases the tendency for breath-holding and laryngospasm at induction of anaesthesia.
Although usually a minor inconvenience, these can be life threatening.
The commonly used volatile anaesthetics are bron-
chodilators, although some such as desflurane have a direct irritant effect on the airways.
Any bronchodilating effects of volatile
anaesthetics are obviously lost when anaesthesia ends.
Lower airway reactivity is also increased in smokers and
mucociliary transport impaired. The forced expiratory volume at 1 s (FEV 1 )
declines in smokers at a rate of around 60 ml yr–1
compared with 20 ml yr–1 in non-smokers.
Also, the closing
capacity ( i.e. lung volume at which airways collapse and trap air) is increased.
Smokers have a greater degree of shunt under
anaesthesia, even when changes in functional residual capacity and closing capacity are accounted for. This is presumably due to altered regional pulmonary mechanics.
These changes, in
addition to the changes in respiratory mechanics that occur with both surgery and anaesthesia itself, make hypoxia more likely both during and after operation.
The relative risk of postoperative pulmonary complications in smokers versus non-smokers is around six.
The absolute values vary between studies (5–25%
non-smokers, 22–57% current smokers). Passive smoking has recently been identified in kids
4.3 Stopping smoking
Years Reduction in lung cancer, chronic obstructive pulmonary disease, ischaemic heart disease, cerebrovascular disease
GP, society, government
5–6 months
Reduction of postoperative complications
GP, surgeon
1 month
Possible increased risk of postoperative pulmonary complications
GP, surgeon
2–10 days Improvements in upper airway reactivity Anaesthetist, surgeon, nurses in pre- admission clinics
12–24 h
Clearance of carbon monoxide
Anaesthetist, surgeon, nurses
5.1 Joints involved in rheumatoid arthritis and implications of these on anaesthesia
RhA is characterised by a chronic symmetrical polyarthritis of (mainly) peripheral joints, especially the fingers, elbows, ankles, but also more proximal joints, shoulders, neck, knees, hips.
Any of these may be relevant to anaesthesia as they may be the focus of an operation and so dictate the choices of anaesthetic technique.
Also, the involvement of any joint may make positioning for regional anaesthesia problematic.
> > Temporomandibular joint:
may impact on mouth opening and, hence,
ease of intubation.
May necessitate fibreoptic intubation.
> > Cricoarytenoid joint fixation:
may cause preoperative hoarseness.
Minimal oedema may therefore cause airway obstruction postoperatively.
>> Atlantoaxial subluxation: assess range of movement and symptoms whilst the patient is awake. Excessive movement (such as with airway management) can cause cord compression. May necessitate fibreoptic intubation.
> > Cervical ankylosis:
causing limited neck extension, difficult airway.
> > Costovertebral and costotransverse joints:
restrictive lung defect.
> > Small joints of hand: limited ability to manage PCA.
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
A + B
Airway:
» Difficult airway for reasons detailed in part (a).
Respiratory:
» Fibrosing alveolitis causing restrictive defect.
> > Pleurisy with effusion.
> > Nodules.
> > Costochondral disease causing
reduced chest wall compliance.
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
CVS
Cardiovascular:
» Pericarditis and pericardial effusions, rarely leading to tamponade, usually
gradually restrictive and requiring pericardectomy.
» Rheumatoid nodules in any layer of the heart, damaging valve function,
causing conduction defects, rarely congestive cardiac failure.
» Increased atherosclerosis and coronary artery disease
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
Neurological
Neurological:
» Peripheral neuropathy due to:
• Peripheral nerve entrapment
(carpal tunnel, ulnar, lateral popliteal).
- Mononeuritis multiplex due to vasculitis.
- Drug treatment.
> > Autonomic dysfunction:
blood pressure and heart rate lability,
gastric paresis.
> > Compression of nerve roots
due to spinal involvement
(especially cervical spine).
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
Endocrine
Chronic steroid use:
compromises glucose tolerance, may ultimately
result in diabetes.
Consider the need for perioperative replacement, effect on immune function, skin fragility.
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
Haematology:
Haematology:
» Normochromic, normocytic anaemia of chronic disease.
> > Iron deficiency anaemia due to chronic gastrointestinal losses with NSAID treatment.
> > Thrombocytosis due to inflammation.
> > Bone marrow depression due to disease-modifying anti-rheumatic drugs (DMARDs).
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
Immune, infection:
Cutaneoumusculoskeletal:
Immune, infection:
» Increased susceptibility to infection
due to DMARDs or TNF inhibitors.
Cutaneoumusculoskeletal:
» Friable skin (due to chronic steroid loss), risk of damage with dressings for cannulae, handling.
> > Fixed joint deformities – care with positioning
5.2 Which systemic features of RhA may be elicited during preoperative assessment? (10 marks)
Renal
Renal:
» Chronic inflammation may cause amyloidosis.
> > Drug treatments may cause CKD.
> > CKD affects metabolism of drugs used perioperatively.
Hepatic:
» Methotrexate may cause liver cirrhosis,
which will impact on drug metabolism.
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (6 marks)
Full blood count
Full blood count:
» Neutropaenia: should not continue with elective surgery if the patient is currently neutropaenic.
> > Anaemia: further investigations may be indicated to determine the underlying cause.
Efforts should be made to correct
anaemia before major surgery.
> > Platelet level: impacts on
feasibility of neuraxial technique.
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (6 marks)
Renal function:
Renal function:
> > Elevated urea, creatinine, reduced glomerular filtration rate – chronic kidney disease may occur due to drugs or the disease itself.
Liver function tests:
» Transaminases and alkaline phosphatase
may rise in active disease.
> > Derangements in all liver function tests may occur due to liver cirrhosis caused by methotrexate.
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (6 marks)
ECG
CXR
ECG:
» Conduction disorders.
» Left ventricular hypertrophy.
Chest x-ray:
» Indicated if there are respiratory symptoms. May reveal pleural effusions, infection, fibrotic lung disease, nodulosis.
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (6 marks
PFTS
» If respiratory symptoms.
Usually reveals a restrictive pattern.
Echocardiogram:
» If a murmur is noted or there are symptoms or signs to suggest poor cardiac function.
Regurgitant valves may be due
to nodulosis or pericardial fibrosis
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (
Other tests
24-hour ECG tape:
» If the patient has palpitations
that cannot be diagnosed on resting ECG alone.
Arrhythmias may be due to
nodulosis of the conduction pathways.
Nasendoscopy and ENT assessment:
» If there is preoperative hoarseness of the voice or other indicator of airway limitation.
Flexion/extension x-rays or MRI of the cervical spine:
» If the patient has pain or neurological symptoms on neck extension or
flexion.
c) Outline the preoperative investigations that are specifically indicated in this patient and the derangements that each may show. (
FBC
U+E
LFTs
ECG
PFTS
Holter
Echo
Nasendocospy
Flexion extension XR / MRI C spine
4.4 Management Bronchsospasm
a) List the factors that may have contributed to an increase in the prevalence of asthma in developed
countries in the last 20 years. (5 marks)
> > Better identification of cases, influenced by targets for asthma management in primary care.
> > Hygiene hypothesis: cleaner environment associated with increased rates of allergy-associated asthma.
> > Obesity: increases an individual’s risk due to altered airway mechanics and chronic inflammatory state.
> > Urbanisation.
> > Asthma development following survival from premature birth.
> > Increased use of drugs such as beta-blockers, NSAIDs, aspirin.
4.4 b) What are the possible causes
of acute bronchospasm during
general anaesthesia in a patient
with mild asthma? (5 marks)
> > Pre-existing upper respiratory tract infection,
poor asthma control, smoking.
>> Airway irritation: cold inspired gases, airway secretions, airway suctioning, laryngoscopy, intubation, extubation, aspiration, carinal stimulation or endobronchial intubation.
> > Drugs causing histamine release,
muscarinic block or allergy.
> > Vagal stimulation:
peritoneal or visceral stretch etc.
4.4 c) Outline the immediate management of acute severe bronchospasm in an intubated patient during general anaesthesia. (10 marks)
General
a
This is an emergency situation and I would alert the theatre team, call for help and assess and manage the patient simultaneously following an ABC approach.
> > Stop surgical/drug triggers where possible.
> > A: Ensure ETT patent, ensure position is correct (carinal or endobronchial placement may have triggered bronchospasm), suction if required
(avoiding stimulation of trachea), 100% inspired oxygen.
4.4 c) Outline the immediate management of acute severe bronchospasm in an intubated patient during general anaesthesia. (10 marks)
B + C
> > B:
Auscultate chest,
confirm wheeze or even absence of breath sounds; check SpO2, manually ventilate to assess compliance and apply higher, sustained pressure for ventilation and longer expiratory flow time;
and increase inspired anaesthetic gas concentration.
> > C:
Check heart rate and blood pressure, increase intravenous filling as increasing intrathoracic pressure reduces venous return, reducing cardiac output and causing a tamponade-type effect.
4.4 c) Outline the immediate management of acute severe bronchospasm in an intubated patient during general anaesthesia. (10 marks)
> > Drugs:
> > Drugs:
• Salbutamol MDI via airway adaptor on breathing circuit, 10 puffs.
• Salbutamol IV 100–300 mcg bolus in extremis/5–20 mcg/min ivi.
• Magnesium 1.2–2 g/20 min IV bolus.
• Adrenaline IV 0.2–1 mg bolus in extremis/1–20 mcg/min ivi.
• Hydrocortisone 200 mg IV.
4.4 c) Outline the immediate management of acute severe bronchospasm in an intubated patient during general anaesthesia. (10 marks)
Post acute event
> > Once acute situation has resolved, monitor response with arterial blood gas, assess whether safe to proceed with case or whether to abandon,
to keep intubated and take to ICU or whether safe to wake the patient up.
> > Incident reporting.
> > Consideration of need for referral
for optimisation of asthma control.
> > Full explanation to patient and/or family, including a written explanation of what has occurred.
Perioperative management of Steroids
Patients on chronic steroid therapy
should receive their usual preoperative dose of steroids on the day of surgery.
However, existing evidence on the necessity of administering perioperative stress-dose steroids for patients with suspected, or even confirmed, secondary adrenal insufficiency is inadequate to fully support or refute this practice.
If HPAA suppression is a clinical concern, perioperative stress-dose steroid administration appears to carry minimal risk compared to the risk of adrenal crisis.
However, the lack of class A and B evidence makes it controversial as to whether the administration of perioperative stress-dose steroids is the standard of care, even for patients with known HPAA suppression.
Perioperative management of Steroids - up to date
The use of stress doses of glucocorticoids has become a common perioperative practice for patients on glucocorticoid therapy. However, available data suggest that these doses are excessive and unnecessary in most patients.
The current approach is to determine glucocorticoid coverage based upon the patient’s history of glucocorticoid intake and likelihood of hypothalamic-pituitary-adrenal (HPA) axis suppression, as well as the type and duration of surgery.
Nonsuppressed HPA axis –
For patients who have been taking exogenous glucocorticoids of any dose for less than three weeks, morning prednisone (<5 mg daily or its equivalent) for any duration, or less than 10 mg of prednisone or its equivalent every other day, we suggest continuing the same glucocorticoid regimen perioperatively
Suppressed HPA axis – For patients who are currently taking prednisone >20 mg/day for three weeks or more and in patients with a Cushingoid appearance, we suggest additional perioperative glucocorticoid coverage, because HPA axis suppression should be assumed to be present
methotrexate: peri op management
Due to its frequent use, management of methotrexate in the perioperative period will be an issue commonly faced by clinicians.
The majority of studies demonstrate safety of methotrexate in the perioperative period; however much of this data comes from retrospective cohort studies.
“Our findings show that discontinuing methotrexate, hydroxychloroquine, leflunomide monotherapy and TNFi plus methotrexate therapy is not associated with increased risk of post- operative infectious complications,” said Dr. Juo. “Therefore, surgeons and rheumatologists should consider continuing medication during the perioperative period to have better control over RA. This will decrease the possibility of requiring steroid therapy and maintain better post- operative functional status.”
Methotrexate side effects and
Gastrointestinal problems, such as nausea, stomach upset, and loose stools
●Stomatitis or soreness of the mouth
●Abnormal liver chemistries, which are typically mild elevations in hepatic transaminases (see ‘Hepatotoxicity’ below)
●A macular punctate cutaneous eruption, which usually occurs on the extremities, often affecting the elbows and knees, but sparing the trunk
●Central nervous system symptoms, including headache, fatigue, malaise, or impaired ability to concentrate
●Alopecia
●Fever, which is drug-related, although fever can also occur due to infection
●Hematologic abnormalities, particularly macrocytosis, in addition to infrequent but severe myelosuppression (see ‘Myelosuppression’ below)
Side effects Steroids
increased appetite – potentially leading to weight gain. acne. thinned skin that bruises easily. increased risk of infections. mood changes, mood swings and depression. diabetes. high blood pressure. osteoporosis (weak and brittle bones)
6.1 Subarachnoid Haemorrhage
Clin features
Sy
The patient typically complains of a
sudden onset or
‘thunder clap’ headache,
described as ‘the worst in my life’.
Associated features include
nausea and vomiting,
neck stiffness,
photophobia,
Sx
focal neurology,
deteriorating level of consciousness,
in severe cases, cardiac arrest.
The differential diagnosis includes
migraine, meningitis, pituitary apoplexy, and
postcoital cephalgia.
6.2 SAH
Pathophysiology
Where
SAH may be due to congenital or acquired con-
ditions, the most common being intracranial
aneurysms which account for 85% of cases.
Other causes include arterio-venous malformations, trauma, and rare conditions such as Moyamoya disease. Hypertension, atherosclerosis, cocaine, alcohol abuse, and smoking increase the risk of SAH.
Most aneurysms occur in the
Circle of Willis close to bifurcations.
The most common sites for rupture
are the posterior communicating artery/
internal carotid artery take-off and
the anterior cerebral artery (Fig.1).
SAH occurs as a result of haemodynamic
stress.
A sudden increase in cerebrovascular arterial pressure results in bleeding into the subarachnoid space with or without intra- ventricular extension
6.2 SAH Investigation to confirm SAH
- Non-contrast cranial computer tomography
(CT) is the first-line investigation and is highly
sensitive (95–100% on the first day) for
detecting blood in the subarachnoid space.
It is also useful for the diagnosis of
complications such as
cerebral oedema and
hydrocephalus.
- Magnetic resonance imaging with
haemosiderin-sensitive sequences (gradient
ECHO or T2-eighted) is also diagnostic but is
rarely performed because of the logistical difficulties involved. - In patients with a high index of suspicion for SAH and a normal CT scan, a lumbar puncture is indicated.
This should be performed 12 h after the onset of symptoms.
Four tubes of cerebrospinal fluid are taken, and
the first and last sent for a red blood cell count,
bilirubin level, and xanthochromia.
- A CT angiogram may be performed to identify the cause of an SAH. It has a negative
predictive value of 82–96% for detecting
aneurysms and is most sensitive for those >4mm in size. - Digital subtraction angiography (DSA)
is the gold standard for diagnosing cause
4.3 Grading
The most frequently used are the Hunt
and Hess and the World Federation of Neurosurgeons Scale (WFNS) which are both clinical scales, and the Fischer scale which is CT-based
Most scales are subject to inter- and
intra-observer variability but do provide a means of communication between teams, and also prediction of prognosis.
The most important predictor of both death and disability is presenting level of consciousness, and, of disability only, a hemiparesis or dysphasia
Acute management SAH
principles
A
Initial management is similar to that for other forms of acute brain injury and focuses on cardiorespiratory stabilization to maintain cerebral perfusion and oxygenation.
This is achieved by securing
the airway, controlling ventilation, and careful arterial pressure management.
PaO2 of 13 kPa
and normocapnia (4.5–5.0 kPa)
is the initial ventilatory target.
In addition, attention must be paid
to minimizing the risk of re-bleeding
and secondary brain injury.
Indications for tracheal intubation include:
1 unconsciousness (GCS <8),
2 reduction in GCS of 2 points,
3 optimization of oxygenation and ventilation,
4 control seizures †
5 protection of the airway in the
absence of laryngeal reflexes
Acute management SAH
C
Extreme hypertension must be treated
in patients with an un- secured,
recently ruptured aneurysm.
A systolic arterial pressure <160 mm Hg
(MAP 110 mm Hg) has a
lower risk of re-bleeding
and should be the aim.
Hypotension (systolic arterial pressure <100 mm Hg)
must be avoided.
Acute management SAH
D
Regular neurological observations,
including pupil size and reactivity
(pre- and post-intubation),
analgesia,
normothermia,
and glycaemic control,
are essential, and,
once the diagnosis is confirmed,
the patient should be referred to a
neuroscience centre.
Critical care Mx SAH
After securing of the aneurysm, the intensive care management of SAH involves treatment of acute complications, optimization of systemic physiology, and the prevention or treatment of delayed neurological deficit (DND) and non-neurological complications.
Aggressive treatment by a multidisciplinary team is associated with improved outcome.
With the shift to early securing of ruptured aneurysms, DND is now the main cause of death and disability after SAH. DND is any clinically detectable neurological deterioration after initial stabilization, with the exception of re-bleeding.
It may be due to delayed cerebral ischaemia (DCI),
hydrocephalus, cerebral oedema, fevers, seizures, and electrolyte abnormalities
Preoperative assessment of a patient posted for aneurysm clipping
The main steps in preoperative evaluation are as follows:
Assessment of the patient’s neurologic condition and clinical grading of the SAH.
A review of the intracranial pathologic condition by evaluating CT for evidence of raised ICP.
Evaluation of other systemic functions, premorbid as well as current condition, with emphasis on systems known to be affected by SAH.
Communication with the neurosurgeon regarding positioning and special monitoring requirements.
Optimization of the patient’s condition by correcting any existing electrolyte disturbances which are quite common in aneurysm patients.
Intraoperative Considerations
Any sudden rise in blood pressure during tracheal intubation can result in rupture of aneurysm. Therefore, the goal during induction of anesthesia is to reduce the risk of aneurysm rupture by minimizing the transmural pressure (TMP) while simultaneously maintaining an adequate cerebral perfusion pressure (CPP).
Blood pressure management should be done taking into account patient’s clinical grade and baseline blood pressure values.
Uptodate - anaesthetic management
A primary goal for anesthesia for these procedures is hemodynamic stability, avoiding hypertension and aneurysmal rupture while maintaining cerebral perfusion. An arterial catheter should be placed prior to induction of anesthesia to allow continuous blood pressure (BP) monitoring. (See ‘Monitoring’ above.)
- Unruptured aneurysms and ruptured aneurysm with suspected normal intracranial pressure (ICP) (ie, normal neurologic examination) – Aim for systolic BP ≤ the patient’s normal systolic BP, maximum 140 mmHg, and mean arterial pressure (MAP) ≥60 mmHg.
- Ruptured aneurysm with suspected or known intracranial hypertension – Passive hypertension should not be treated. Hypertension in response to noxious stimulation and iatrogenic hypertension due to vasopressors should be avoided, and cerebral perfusion pressure (CPP) ≥50 to 60 mmHg should be maintained. (See ‘Blood pressure goals’ above.)
●A temporary clip may be placed on a feeding vessel to facilitate dissection and permanent clipping. During longer clip times, or if neuromonitoring shows ischemic changes during temporary clipping, increasing MAP by 10 to 20 percent may be appropriate. (See ‘Temporary clipping’ above.)
●Induced hypothermia has not been shown to improve outcomes for patients who undergo aneurysm clipping. (See ‘Temporary clipping’ above.)
●Adenosine may be administered to induce temporary bradycardia or cardiac arrest to reduce or suspend flow through the aneurysm as an alternative to temporary clipping, or in the event of intraoperative aneurysm rupture. (See ‘Adenosine-induced temporary flow arrest’ above.)
Up To Date SAH
Endovascular procedures
Concerns specific to endovascular procedures used to treat intracranial aneurysms include the following:
●Intra-arterial BP monitoring is required for these procedures. The femoral sheath placed for the procedure may be used for BP monitoring in lieu of a peripheral arterial catheter.
●Endotracheal intubation is often the most stimulating part of the case. Hypertension should be attenuated by deepening anesthesia with propofol (20 to 50 mg IV), lidocaine (1 mg/kg IV), or fentanyl (100 mcg IV), or by administering esmolol (0.5 to 1 mg/kg IV) prior to intubation.
●Patients are frequently heparinized for these procedures. The goal range for activated clotting time (ACT) and the procedure for performing ACTs should be established with the interventionist.
●Oral administration of antiplatelet medication may be required intraoperatively. An orogastric tube should be placed after intubation for administration of aspirin or clopidogrel.
●Aneurysmal rupture is uncommon during endovascular procedures but is most likely with deployment of the initial coil [23]. In the event of rupture, heparinization should be reversed with protamine. Patients should be managed as described above. (See ‘Rupture prior to aneurysm exposure’ above.)
●Downstream thromboembolism may complicate endovascular coiling and is detected by angiography.
If thromboembolism occurs during coiling, abciximab, a glycoprotein IIb/IIIa inhibitor, may be administered (bolus dose of 0.25 mg/kg IV, followed by an infusion of 0.125 mcg/kg/minute to a maximum dose of 10 mcg/minute). Some recommend inducing hypertension after the aneurysm is secured, as treatment for thromboembolism and resultant cerebral ischemia.
7.1
Severe Pre-Eclampsia
Define.
Pre-eclampsia is new hypertension
(systolic greater than 140 mm Hg,
diastolic greater than 90 mm Hg)
presenting after 20 weeks’ gestation with
significant proteinuria.
(Significant proteinuria:
24-hour urine collection greater than 300 mg protein
OR urinary protein:creatinine ratio
[PCR] greater than 30 mg/mmol).
Pre-eclampsia occurs in 2–3% of
all pregnancies and is more common
in primigravida
7.1 Pre-Eclampsia
Incidence
Risk factors
Pre-eclampsia occurs in 2–3% of all pregnancies
and is more common in primigravida
or the first pregnancy with a particular partner.
Other risk factors include a positive family history, pre-existing hypertensive disease, diabetes mellitus, multiple pregnancy, increasing maternal age and obesity
7.1 Severe Pre-Eclampsia
Severe pre-eclampsia is defined as any one of the following occurring after the 20th week of pregnancy:
(i) severe hypertension
(systolic blood pressure > 160 mmHg
or
diastolic blood pressure > 110mmHg);
(ii) proteinuria > 5 g per 24 h;
(iii) oliguria < 400 ml per 24 h;
(iv) cerebral irritability;
(v) epigastric or right upper quadrant pain (liver capsule distension); or
(vi) pulmonary oedema.
7.1 Eclampsia
Eclampsia is the occurrence of convulsions
in a woman with pre-eclampsia.
This only occurs in about 1 in 2000 deliveries in the
industrialised world but the incidence is much
7.1 Pre-Eclampsia
Symptoms to report immediately
Symptoms to report immediately:
> > Severe headaches.
> > Visual disturbance, blurred vision, flashing lights.
> > Sudden swelling of hands, feet or face.
> > Upper abdominal pain or vomiting.
7.2 Severe PET b) How should this patient be
managed following admission to
your labour ward? (12 marks)
Multidisciplinary management is required of this
obstetric emergency, with obstetric, midwifery, anaesthetic and intensive care input.
Level 1 care as a minimum.
Assess and manage the patient simultaneously following a systems-based approach:
ABCDE etc
7.2 Severe PET b) How should this patient be
managed following admission to
your labour ward? (12 marks)
a+b
> > Airway:
• Airway assessment – anaesthesia for urgent delivery or airway support
may be necessary.
• Assess for voice change, hoarseness, facial oedema – laryngeal
oedema and difficult intubation are more likely.
> > Respiratory:
• Pulmonary oedema may
result in respiratory compromise.
- Assess oxygen saturations, respiratory rate.
- Auscultate chest.
- Supplementary oxygen if required.
• Consider fluid restriction to
1 ml/kg/h to a maximum of 80 ml/h
(although may need extra
bolus if hydralazine is commenced).
7.2 Severe PET b) How should this patient be
managed following admission to
your labour ward? (12 marks)
C
> > Cardiovascular:
• Cannulate.
Start antihypertensive medication to target BP
less than 150/100:
first line oral or intravenous labetalol;
second line intravenous hydralazine;
third line oral nifedipine.
• Monitor response with frequent
blood pressure checks.
7.2 Severe PET b) How should this patient be managed following admission to your labour ward? (12 marks)
Neuro + GI
> > Neurological:
• Assess for hyperreflexia,
severe headache,
Visual disturbance.
~
May signify risk of eclampsia.
Consideration of magnesium treatment if
these symptoms are present or
if there is significant proteinuria.
> > Gastrointestinal:
• Keep nil by mouth and administer antacid in view of likely imminent delivery and possibility of seizure.
7.2 Severe PET b) How should this patient be managed following admission to your labour ward? (12 marks)
Haematological
Renal
Hepatic
> > Haematological:
• Check full blood count for
platelet level and coagulation screen.
> > Renal:
• Urinary protein:creatinine ratio and
urine dip for protein to assess
disease severity.
- Monitor urine output.
- Monitor renal function.
> > Hepatic:
• Check transaminases and bilirubin.
7.2 Severe PET b) How should this patient be managed following admission to your labour ward? (12 marks)
Obs
> > Obstetric:
• Continuous fetal monitoring with cardiotocograph, especially once
antihypertensives are initiated.
• Uric acid is a marker of disease severity.
• Plan for delivery: baby is at term and ultimate cure for pre-eclampsia is
delivery of the placenta
7.3 c) What changes would you make to your usual general anaesthetic technique for a pregnant woman
if this woman needed a general anaesthetic for caesarean section? (5 marks)
A+B
> > Airway:
- Increased awareness of risk of and preparation for difficult airway: assess for upper body or facial oedema and hoarseness that may indicate oropharyngeal and laryngeal oedema.
- Airway oedema may worsen over duration of surgery: deflate endotracheal tube cuff to check for leak before extubation.
> > Respiratory:
• Limit fluid input to 80 ml/h unless matching losses through e.g. haemorrhage.
• Higher airway pressures and PEEP may be required for oxygenation in the presence of pulmonary oedema – this may necessitate postoperative ventilation as well.
7.3 c) What changes would you make to your usual general anaesthetic technique for a pregnant woman
if this woman needed a general anaesthetic for caesarean section? (5 marks)
CVS + Pharm
> > Cardiovascular:
• Consideration of intra-arterial blood pressure monitoring.
• Mitigate pressor response of intubation with short-acting opioid, e.g. alfentanil 10 mcg/kg.
• Consider pressor response of extubation if blood pressure remains high and labile.
Consider short-acting beta-blocker,
e.g. labetalol 10–20 mg intravenously.
> > Pharmacology:
• Caesarean section under general anaesthesia has an increased association with uterine atony. Ergometrine is contraindicated for this patient due to its hypertensive effect.
7.3 c) What changes would you make to your usual general anaesthetic technique for a pregnant woman
if this woman needed a general anaesthetic for caesarean section? (5 marks)
Neuro
Renal
> > Neurological:
• Even more important to ensure adequate pain relief before waking due to impact of circulating catecholamines on blood pressure.
Consider transverse abdominis plane blocks and morphine.
• Magnesium prolongs the effect of depolarising and non-depolarising muscle relaxants: mandatory use of nerve stimulator, and anaesthesia may have to be prolonged to allow for this prolonged offset time.
> > Renal:
• Avoid NSAIDs due to the effect of pre-eclampsia on kidney function
7.4 Define HELLP syndrome
HELLP syndrome
The haemolysis, elevated liver enzymes and low platelet (HELLP) syndrome describes the
combination of
- Microangiopathic haemolytic anaemia,
- thrombocytopaenia and
- hepatic ischaemia with
periportal haemorrhage
and necrosis
which can occur with severe pre-eclampsia.
7.4 HELLP syndrome
a/w
HELLP syndrome is associated with an increased risk of developing other serious complications of pre-eclampsia ( e.g .seizures)
and both maternal and fetal mortality is increased.
After onset, the syndrome worsens
rapidly for 24–48h
but usually resolves within 6 days
Partial HELLP may be diagnosed if only 1 or 2 of the criteria are pre-sent.
Occasionally, it may occur when hypertension or proteinuria is absent or minimal;
20% of cases present post-partum.
It may present with
epigastric/right hypochondrial pain,
malaise, nausea and vomiting.
It may be asymptomatic and
revealed by detecting hypertension
on routine checking.
Management of pre-eclampsia
Early diagnosis, control of blood pressure, prevention of convulsions and timely delivery are the goals of management.
A heightened awareness of pre-eclampsia as a possible diagnosis is necessary because of its variable presentation. Close monitoring is essential in severe or unstable pre-eclampsia.
Good intravenous access is essential in all cases because of the risk of complications,
particularly haemorrhage and convulsions.
The level of monitoring should be tailored to each
individual patient. Blood pressure should be frequently measured and invasive monitoring may be necessary in unstable patients.
Fluid balance should be meticulously recorded and
central venous pressure (CVP) monitoring may be required if there is any uncertainty regarding volume status.
Peripherally inserted central catheters are safer in patients with existing or potential coagulation abnormalities. Studies have shown a
poor correlation between CVP and left atrial pressure in
severe pre-eclampsia, particularly at pressures > 6 mmHg.
Therefore, pulmonary artery catheters may be needed in some cases, although these in themselves are associated with maternal morbidity and mortality and careful consideration should be given to their use.
lol
Full blood count, urea, electrolytes and
7.4 Management of HELLP
Management of HELLP
This is the same as for pre-eclampsia. Meticulous and frequent
monitoring of the cardiovascular system, haematological status
and renal and hepatic function is required with supportive thera-
py as indicated by the measured parameters. Changes in haema-
tological state may occur rapidly and require aggressive treat-
ment (in discussion with a haematologist)
GA management PET
General anaesthesia
Problems associated with general anaesthesia in pre-eclampsia include an increased risk of difficult intubation (oedema of the upper airway) and cardiovascular instability, in addition to
the usual risks associated with pregnancy.
Convulsions may occur during operative delivery and some would argue that these are easier to manage under general anaesthesia.
General
anaesthesia will be required for emergency Caesarean sections,
in the case of failed regional techniques or if the latter
are contra-indicated.
The airway should be fully assessed prior to induction with regards to the airway. Signs of upper body oedema, especially facial, are particularly worrying. Awake intubation may be considered to be the safest approach, although nasal intubation can
precipitate significant bleeding
(venous engorgement, disordered
coagulation).
Bleeding may also occur with oral intubation.
Drugs used to obtund the hypertensive response to laryngoscopy and intubation include magnesium sulphate 40 mg kg -1 , short- acting opioids
(e.g. alfentanil 10μg kg–1),
β-blockers (e.g. esmolol 0.5 mg kg–1
or labetalol 10–20 mg) and
lidocaine (1.5 mg kg–1 given 5 min prior to intubation).
Extubation may also cause an exaggerated cardiovascular response which should be
attenuated. Esmolol or lidocaine are logical choices. It is impor-tant to remember that magnesium will prolong the effects of depolarising and non-depolarising neuromuscular junction blockers and reduce the fasciculations when succinylcholine is
given. Nerve stimulators should be used in all cases. Laryngeal
oedema may worsen during the operation and, prior to extubation, the endotracheal tube cuff should be deflated to ensure that there is still air leaking around the tube
8.1 Pain
Define Acute Pain
“An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage,
or described in terms of such damage’.
Acute pain lasts <3months
8.1 b
Define Chronic Pain
Chronic pain last greater than 3 months
8.2
CVS physiological effects of pain
Direct effects include:
increased heart rate,
stroke volume and
peripheral resistance,
which increase myocardial oxygen demand.
The increased heart rate decreases
diastolic filling time,
which can decrease coronary blood flow
and oxygen delivery.
Indirect effects of severe acute
pain cause activation of the stress response. Sympathetic activation and
catecholamine release can cause epicardial vasoconstriction and reduced coronary artery diameter,
further increasing the risk of myocardial ischemia.
Other indirect effects cause increased coagulability, which increase the incidence of thromboembolism and increase the risk of acute thrombosis of vascular grafts
8.3 b
Neuroendocrine physiological effects of pain
The basic physiologic effect of pain
on the endocrine system is one of severe stress.
Pain initially stimulates the HPATG system
to produce and secrete extra hormones from the adrenals, gonads, and thyroid.
Hormones, including cortisol, pregnenolone, DHEA, testosterone, and thyroid (T3 and T4) travel from their producing glands to distinct tissue targets, including injured nerves and the CNS.
Hormones provide immunologic, anti-inflammatory, and regenerative properties for cellular protection and healing. In the stimulation phase of severe pain, serum hormone levels are elevated. If pain persists unabated for too long, the hormonal system is unable to tolerate the stress of pain, and hormone production may be decreased causing serum hormone levels to drop below normal.
The most serious hormone complications of severe chronic pain are hyper- and hypocortisolemia.
Cortisol serum levels rise and fall with emotion, exercise, nutrition, and disease states.
Exercise is well known to positively modify cortisol levels, and this activity is highly recommended in pain patients.
8.4
Methods to reduce post- op opioid consumption
Pre Op
Consider preoperative dose of gabapentinoids
Continue usual medication as long as possible ()
Intraoperative measures
- Regional anaesthesia plus GA
- Option of intrathecal local anaesthesia plus opioid, or an epidural bolus
- Nitrous oxide
- Consider local anaesthetic infiltration to wound by surgeon
- Consider lidocaine infusion
Postoperatively
- Epidural infusion
- Consider wound catheter with local anaesthetic
- Adjuncts: paracetamol 1g regularly, max 4g/ day (caution: co-codamol)
- Consider short course (48 hours) NSAIDS
8.5
Define opioid induced hyperalgesia
A state of nociceptive sensitization
caused by exposure to opioids.
The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli.
8.6 Define tolerance
The diminishing effect of a drug resulting from repeated administration at a given dose
9.1 Factors to consider for Day-case suitability
- Is the operation an appropriate day-case procedure?
- Is there anything we would do for this patient by admitting themovernight which could not be done at home?
- Are the patient’s home circumstances adequate for day surgery discharge
9.1 Surgical factors for Day case surgery
- The procedure should not have significant risk of major post-operative complications necessitating immediate medical intervention
(haemorrhage, cardiovascular instability). - No prolonged specialist postoperative care or observation required.
- Abdominal and thoracic cavities should only be opened with minimally invasive techniques.
- Postoperative pain should be controllable with oral analgesia + regional anaesthesia techniques.
5 .Patient should be able to rapidly resume normal functions (oral nutrition, safe mobilization).
- Urgent procedures are also appropriate for a semi-elective day-case pathway, for example, drainage of abscesses, some trauma surgery
9.1 Medical factors for Day case
- Patients with stable chronic medical conditions such as diabetes, asthma, or epilepsy are often better managed with minimal disruption to their daily routine as facilitated by day surgery.
- Patients with unstable medical conditions such as unstable angina or diabetes are unlikely to be appropriate for day surgery. However, the question should be asked whether anything other than the most urgent surgery is appropriate in this patient group. If these patients do require urgent surgery, inpatient management is required for perioperative monitoring.
- Obesity: Obese patients benefit from day surgery management with its short-acting anaesthetics and early mobilization. Even morbid obesity is not a contraindication to day surgery.
- While technically challenging, the majority of complications occur during the procedure or in first-stage recovery and resolve early in the recovery period. An overnight stay is unlikely to confer any benefit and in fact day-case bariatric surgery is a developing area.
- The elderly: There is no upper age limit for day-case surgery. Increasing age does not lead to adverse day surgery outcomes and being in their familiar home surroundings may reduce post-
operative cognitive dysfunction. - Paediatrics: Full-term infants over 1 month are generally appropriate to have a day surgery procedure but in ex-premature infants, a higher age limit (60 weeks post-conceptual age) is advised owing to the increased risk of postoperative apnoea.
- Day surgery is particularly appropriate for children, is less disruptive to family life, and is promoted by the European Charter of Children’s rights which advocate that ‘children should be admitted to hospital only if the care they require cannot be equally well provided at home or on a day basis’.
- ASA: ASA grade is not a useful assessment for day surgery suitability with ASA III patients reporting no increase in post operative complications than ASA I or
9.1 Social factors for Day case surgery
- Social factors
24 h home care: It is generally recommended that after a general anaesthetic, most patients should have a responsible adult to accompany them home and remain with them for 24 h after surgery
(this requirement is beginning to be challenged after very minor surgery). Traditionally, this has excluded
those patients living alone from day surgery. Some units
however now deploy carers to patient’s homes to stay overnight enabling even these patients to be treated as day cases.
- Access to a telephone.
- Geographical proximity to hospital; travelling time
> 1 h may be contraindication for certain procedures (e.g. day-case tonsillectomy). - The patient must understand, engage with, and consent to the surgical procedure and for it to be performed as day surgery
9.2 Anaesthetic Mx of Day case surgery
Anaesthetic management
The key requirements of a day surgery anaesthetic agent include:
- rapid onset and offset of anaesthesia with clear-headed emergence,
- minimal postoperative nausea and vomiting (PONV), dizziness,
or drowsiness,
3 rapid return to full cognitive functions.
While these are properties desirable for all anaesthetic techniques, they are particularly important in the day surgery patient due to the requirement for rapid return to oral nutrition, mobilization, and full cognitive function.
The benefits of total i.v. anaesthesia vs
volatile techniques have been debated in many other publications and are beyond the scope of this article; however, the key factors in delivering high-quality
day surgery anaesthesia are attention to detail in all aspects of the anaesthetic technique.
Short-acting agents,
supplemented by local anaesthetic techniques and simple oral analgesia,
protocol-driven use of anti-emetic
medication where required,
minimal starvation times,
and judicious use of i.v. fluids are the key to success.
Day surgery patients have a finite time on the day surgery unit before discharge that same day.
Therefore, prompt management of
pain and nausea and vomiting and
early mobilization are paramount.
A more rapid recovery from anaesthesia results in quicker turnaround, improved patient experience, and reduced costs.
9.2 Day case analgesia
Analgesia
A multimodal approach to pain relief should be adopted for day surgery patients. This discussion is beyond the remit of this article, but the key facets are:
†
Regular oral analgesia with paracetamol combined with long acting non-steroidal anti-inflammatory drugs, if not contraindicated
†
Supplementation with local or regional anaesthesia where possible.
†
Avoidance of any long-acting opiates and judicious use of short-acting opiates if required for management of acute pain
9.2 Day Case Postoperative nausea and vomiting
Postoperative nausea and vomiting
PONV should be risk assessed before operation and prophylactic anti-emetics given to patient stratified at high risk. Policies should also exist for the rapid management of any postoperative PONV as
this can significantly delay discharge. The routine use of i.v. fluids can enhance a patients feeling of well-being and reducing PONV
9.3 Nurse led discharge checklist
Vital signs stable
Orientated to time, place, and person
Passed urine (if applicable)
Able to dress and walk (where appropriate)
Oral fluids tolerated (if applicable)
Minimal pain
Minimal bleeding
Minimal nausea/vomiting
Cannula removed
Responsible escort present
Has carer for 24 h postop
Written and verbal postop instructions
Knows who to contact in an emergency
Follow-up appointment
Removal of sutures required?
Referrals made
Dressings supplied
Patient copy of GP letter
Carbon copy of consent
Sick certificate
Has take home medication Next dose:
Information leaflet for tablets
Postop phone call required?
9.3 Nurse led discharge
Nurse-led discharge is key to day surgery and should include:
†
1. Timely discharge once all the recovery milestones have been met (
- Information for the patient and their carers regarding what to expect and their responsibilities, so they may go home feeling confident.
3 Appropriate analgesia with written instructions given to the patient. Procedure-specific protocols for take-home analgesia are recommended.
- A discharge summary should they require medical assistance overnight.
- A telephone number where patients can access advice from a senior nurse overnight should they require it. This person must be able to give advice relating to complications of the surgical procedure undertaken.
10.1 Neuraxial Blockade
CVS benefits of neuraxial blockade
???
?????
Hypotension
These two effects result from the sympathetic block that accompanies spinal anesthesia, and from block of adrenal medullary secretion.
Bradycardia are direct (blockade of sympathetic cardioaccelerator fibers) and indirect. Indirect mechanisms include decreased output of the myocardial pacemaker cells due to decrease in venous return, stimulation of low-pressure baroreceptors in the right atrium and vena cava, and stimulation of mechanoreceptors in the left ventricle resulting in bradycardia (paradoxical Bezold-Jarisch reflex)
10.1
Haematological benefits of neuraxial blockade
????
- 2 Name the layers traversed by needle for a subarachnoid block
- Skin
- Subcutaneous fat
- Supraspinous ligament
- Interspinous ligament
- Ligamentum flavum
- Dura mater
- Subdural space
- Arachnoid mater
- Subarachnoid space
10.3 a Absolute contraindications
- Patient refusal
- Infection at the site of injection
- Uncorrected hypovolemia
- Allergy
- Increased intracranial pressure
10.3 b Relative Contraindications
- Coagulopathy
- Sepsis
- Fixed cardiac output states
- Indeterminate neurological disease
