Section 2 Flashcards
HistoRY You are called to see a 17-month-old male child who is currently in
the children’s ward.
He was brought into Accident and Emergency by his mother due to grunting and
looking red in the face. Two hours earlier he was eating ‘Bombay mix’ when he
had an episode of coughing and went blue. Shortly afterwards he recovered and
was well enough to eat a banana and chocolate biscuit
Past Medical History Full-term normal delivery
Vaccinations up-to-date
No previous anaesthetics
on examination Playing in the ward
Temperature: 37°C
Spo2: 94% on air
Respiratory rate: 22/min
on auscultation: harsh breath sounds on the left with some basal
crepitations
investigations Chest X-rays provided
summarise the case.
What are the anaesthetic
concerns?
• Paediatric case
• Risk of aspiration (Wait until fasted—not urgent)
• Possible chemical pneumonia
What are the signs of respiratory
distress in children?
explain the cXRs.
X-ray on inspiration
• Minimal hyperinflation seen on the left lung
• No foreign body (FB) seen
X-ray on expiration
• Hyperinflation of the left lung.
• In both inspiration and expiration images the diaphragms have not
moved.
• FB—not seen on the X-ray.
explain pathophysiology of hyperinflation (ball-valve mechanism).
• On inspiration both lungs will tend to appear similar in terms of their degree of aeration. The reason for this is that the trachea and bronchi normally widen on inspiration, allowing passage of air into the affected lung past the foreign body.
• On expiration the foreign body can obstruct the bronchi as the diameter of the bronchi decreases slightly on expiration. The greatest difference in lung aeration will therefore be seen on the expiration image as air is exhaled from the normal lung (right lung) but not from the affected lung (left lung).
it was planned to take this child to theatre for eUA for removal of foreign body. Would you use any premedication in this child? if yes,
what would you prescribe?
Antisialogouges
Atropine/Glycopyrollate
• Atropine dose 20–40 mcg/kg PO; max dose 500 mcg
Pros: reduce secretions, so reduces suctioning during bronchoscopy, vagolytic
Cons: thickening of mucus
eMLA/Ametop
• EMLA: 2.5% lidocaine and 2.5% prilocaine (leave it on for 45–60 minutes)
• Ametop: Amethocaine (leave it on for 30–45 minutes); causes
vasodilatation
What is the particular issue with peanuts as a foreign body?
These biological substances fragment and cause irritation and chemical pneumonia.
Explain the anaesthetic management pediatric foreign body aspiration.
• Preoperative assessment—anaesthetic and medical history, allergy and starvation status
• A, B, C
• Explain conduct of anaesthesia and consent parents
• Bronchoscopy should be postponed because child is not compromised.
inform
Trained assistant, senior anaesthetist check
• Anaesthetic equipment, airway equipment
• Anaesthetic and emergency drugs
Anaesthetic plan
• Inhalational induction with spontaneous ventilation (sevoflurane + oxygen)
• Avoid N2o (because of hyperinflated lung)
• Prior to bronchoscopy spraying of pharynx and vocal cords with 10% lignocaine (Max. 3 mg/kg, 1 puff = 10 mg)
• Can intubate as it gives surgeon an idea of the size of scope and avoids unnecessary trauma
• The correct size of scope is one which allows an audible leak of 20 cm H2o
• Maintain spontaneous breathing with a T piece attached to a side piece in the bronchoscope
• A small dose of neuromuscular blocking agent or propofol to aid extraction of the foreign body through the cords
• Once the procedure is finished, a tracheal tube can be inserted if a full stomach is considered a problem, and the patient woken up and extubated once protective reflexes have returned.
• Analgesia not usually required as the procedure is not painful.
Paracetamol can be given as required.
What are the different types of
bronchoscopes?
• Rigid: STORZ ventilating bronchoscope, Venturi scopes
• Flexible: Fibreoptic scope (Dormia basket can be used to extract foreign
body)
What are the complications of bronchoscopy, particularly with rigid bronchoscopes?
Trauma to lips, teeth, base of tongue, epiglottis, and larynx.
• Damage to the tracheobronchial tree is rare but causes pneumothorax, pneumomediastinum, and surgical emphysema.
• Haemorrhage is usually minor and settles spontaneously.
The child is in recovery. The nurse is concerned as he is tachycardic and in respiratory distress.
What are the differential diagnoses?
• Residual anaesthetic
• Hypothermia
• Hypovolemia
• Hypercarbia
• Laryngospasm
• Aspiration
• Anaphylaxis
• Barotrauma
An X-ray is done in recovery.
see Figure 2.3. What is your
diagnosis?
Barotrauma and right-sided pneumothorax with mediastinal shift.
What are the clinical signs you would expect in a child with pneumothorax?
• Hypoxic
• May be shocked
• Decreased air entry and hyper resonance on affected side
• Distended neck veins
• Later, trachea deviates away from affected side
How would you manage?
• High flow oxygen via reservoir mask
• Immediate needle thoracocentesis to relieve tension
• Chest drain urgently to prevent recurrence
After he recovers, he is thirsty.
Would you give him fluids?
No. It can be given after the lignocaine wears off; wait at least 1 hour.
A 37-year-old female who is 30 minute postpartum with an epidural
suddenly becomes short of breath and is worsening.
What are possible causes?
Patient factors
• Asthma
• Pulmonary infection
• Anaemia
obstetric factors
• Preeclampsia
• Amniotic fluid embolism (AFE)
• Pulmonary embolism
• Ergometrine use
• Cardiomyopathy
Anaesthetic factors
• High block assuming that the epidural is still being used in this case
Another way to classify the differential diagnoses is to take the obstetric
versus nonobstetric approach.
What is the pathophysiology of AFe?
First described by Steiner in 1941, it is a diagnosis of elimination after other causes of cardiovascular instability and collapse have been rejected. Difficult diagnosis is reflected by a wide ranging incidence of 1:8000 to 1:80 000 deliveries
Pathogenesis
• Embolic: due to an emboli caused by entry of amniotic fluid or fetal cells in the circulation
• Immunological: similar to anaphylaxis as fetal cells are not always present
Presentation
• Occurs usually during labour and delivery (including LSCS) but can occur up to 48 hours post delivery, typically in two phases
• Phase 1: characterised by acute shortness of breath and hypotension followed by cardiac failure, cardiac arrest, pulmonary oedema, acute lung injury, convulsions. and loss of consciousness.
○ The maternal mortality rate is 26%–60%.
• Phase 2: 40% of women who survived the first stage will go on to develop the haemorrhagic phase due to DIC.
What are the risk factors for AFe?
○No proven risk factors, but the following may be associated with a higher risk of developing AFE:
•Advanced maternal age, multiparity, meconium stained liquor, intrauterine fetal death, polyhydramnios, strong frequent or tetanic uterine contractions, microsomia, chorioamnionitis, uterine rupture, and placenta accreta.
What systemic changes occur during AFe?
Haemodynamic changes
• Increase in systemic and pulmonary vascular resistance, resulting in acute pulmonary hypertension, left ventricular dysfunction and pulmonary oedema.
• Myocardial dysfunction results from ischaemia and as a direct depressant effect of endothelin and humoral factors.
Pulmonary
• Vasospasm and ventricular dysfunction lead to hypoxia.
• Survivors develop an ARDS-like picture.
coagulation
• DIC
• Amniotic fluid contains activated coagulation factors II, VII, and X. It induces platelet aggregation, releases platelet factor III, and has a thromboplastin-like effect.
• The clinical picture is one of massive haemorrhage and haemodynamic
collapse.
What is the management of AFe?
○ The management is mainly supportive, invasive monitoring, and transfer to ITU.
Management goals in the operating theatre are
• Maintaining oxygenation—use of PEEP.
• Haemodynamic stability—inotropes are usually required.
• Maintenance of uterine tone.
• Management of DIC—Liaise with haematologist. FFP, cryoprecipitate, and platelets are usually required. Recombinant factor VII has been used in massive haemorrhage.
A 66-year-old previously fit and well male patient had a total hip replacement under a general anaesthetic. In recovery, he is complaining of unilateral eye pain.
What is your differential diagnosis?
ocular causes
•Conjunctivitis
•Corneal abrasion
•Corneal ulceration
•Foreign body
•Trauma
orbital causes
•Glaucoma
•Iritis
•optic neuritis
•Migraine
•Trauma
What are the most common/likely causes of painful eye?
• Corneal abrasion due to mask, eye tape, and decreased tear production
• Chemical injury from antiseptic solutions and drugs
• External pressure resulting in optic neuropathy
• Retinal ischaemia
• Exacerbation of glaucoma
What are the factors that make a patient high risk to attaining an eye injury?
• Position
° Lateral: abrasion/trauma
° Prone: optic nerve pressure/conjunctival oedema
• Pre-existing eye disease
• History of diabetes and hypertension
• Prolonged surgery
What is glaucoma?
Glaucoma is the condition where the free flow of aqueous humour is hindered, which can increase the intraocular pressure (IoP).
• Closed angle
• Open angle
• Normal tension glaucoma
In all types of glaucoma the loss of vision is due to optic nerve damage
What is open- and closed-angle glaucoma?
○ Open-angle glaucoma (chronic glaucoma) is the condition in which aqueous fluid drains very slowly due to clogging of the trabecular mesh.
○ Closed-angle glaucoma, also called acute glaucoma, is an ophthalmologic emergency. •This occurs when the iris completely blocks fluid access to the trabecular meshwork.
•The pressure builds up, causing the patient excruciating eye pain, and vision is lost quickly.
○ In normal tension glaucoma optic nerve damage is present but with normal IoP.
•The cause is mainly familial and history of systemic heart disease such as irregular heart rhythm.
What are the determinants of
ioP? What are the normal
values?
IoP is dependent on
• Contents, such as volume of aqueous, vitreous, and blood
• Scleral compliance
• Tone of extra ocular muscles
• Drainage of aqueous, which depends on venous pressure
Normal IoP = 16+/− 5 mmHg; >25 mmHg is pathological.
can the ioP be normal in
glaucoma?
Yes. In open-angle and normal tension types, the IoP can be normal.
The sclera adapts to increased volume, and hence IoP is normal.
explain the pathophysiology of closed-angle glaucoma.
○ Normally the aqueous humour produced by the ciliary body is drained to the veins through the Canal of Schlemm.
○ If the angle between iris and cornea is acute/blocked, then the drainage is affected, resulting in increased intraocular pressure.
• Pain and loss of sight in extreme conditions; “silent thief of sight”
Avoid drugs that dilate the pupils as this also can close the angle. See
Figure 2.6
What is the effect of
anaesthesia on ioP?
Consider IoP equivalent to ICP and structure your answers similarly. Any
increase in volume and pressure intraocularly and obstruction to venous
drainage would cause an increase in IoP.
• IV induction drugs: decrease IOP except ketamine.
• Muscle relaxants: suxamethonium increases IOP up to 10 mmHg
due to extraocular muscle twitching. This can be overcome by giving
adequate dose of IV induction agents. Nondepolarising muscle relaxants
decrease IoP.
• Hypoxia, hypercarbia, neck ties/coughing: increase IOP
How would you decrease the
ioP in an acute setting?
General
• Head up tilt
• Avoid neck ties/coughing/vomiting, etc.
• Maintain oxygenation, and avoid hypercarbia and hypotension.
Drugs
• Acetazolamide
• Mannitol
• Propofol
can you tell me the pathway of the light and corneal reflexes?
- Pupillary (light) reflex
○ Afferent—Optic nerve, which terminates in the pretectal area of midbrain.
○ Axons from here then radiate bilaterally to terminate in the Edinger-Westphal nucleus
⊙Ciliary ganglion parasympathetic postganglionic axons travel in the short ciliary nerve and end on the iris sphincter.
○ Efferent—Oculomotor nerve
○ Ganglion—Ciliary ganglion
○ Central mediator—Occipital lobe of brain - corneal reflex
○ Afferent—Ophthalmic or nasociliary division of trigeminal nerve trigeminal nerve trigeminal ganglion spinal trigeminal tract spinal trigeminal nucleus
○ Efferent—Facial motor neurons facial nerve branch to orbicularis oculi
○ Ganglion—Trigeminal ganglion
○ Central mediator—Pons
Describe the blood supply of
the spinal cord.
The spinal cord derives its blood supply from a single anterior spinal artery
(ASA), paired posterior spinal arteries (PSA), and by the communicating
segmental arteries and the pial plexus.
AsA
Single artery formed at the foramen magnum by the union of each vertebral
artery. Blood flows centrifugally supplying the anterior two-thirds of the spinal
cord in front of the posterior grey column.
PsA
Derived from the posterior inferior cerebellar artery (PICA) or vertebral artery,
with blood flowing centripetally in this arterial system. The arteries lie along
the postero lateral surface of the spinal cord medial to the posterior nerve
roots.
Pial arterial plexus
Surface vessels branch from the ASA and PSA forming an anastomosing
network that penetrates and supplies the outer portion of the spinal cord.
segmental branches
Segmental or radicular branches arise from various arteries—vertebral, deep
cervical, costo cervical, aorta, and the pelvic vessels.
Arteria radicularis magna, or the artery of Adamkiewicz
Arises from the thoracolumbar part of the aorta, usually on the left, and
enters the spinal cord at the level of L1.
Various regions of spinal cord are vascularised unevenly. The cervical
and lumbosacral parts are well vascularised whereas the thoracic part of
the spinal cord, especially the anterior region, derives the branches from
intercostal and iliac arteries, which vary in location and numbers making it
prone to ischaemic damage. See Figures 2.7 and 2.8.
Describe the venous drainage of the spinal cord.
What is its importance?
○ Radicular and spinal veins drain into the internal vertebral venous plexus and later drain into the azygos system and the superior vena cava.
○ The plexus communicates with the basilar sinus in the brain and with the pelvic veins
and inferior vena cava.
○ So in patients with increased intra-abdominal pressure, blood is diverted from the inferior vena cava to the plexus, leading to engorgement of epidural veins.
a. This increases the risk of accidental venous puncture during the conduct of epidural anaesthesia.
b. It also decreases the effective epidural space volume, thereby requiring a smaller volume of local anaesthetic
Which part of the spinal cord acts as a watershed zone?
○ Watershed effect occurs when two streams of blood flowing in opposite directions meet.
○ This happens where the radicular artery unites with the ASA, where blood courses upward and downward from the entry point, thus leaving a watershed region between the adjacent radicular areas where blood flows in neither direction.
○ The watershed effect is maximum in the mid-thoracic area due to the greater distance between the radicular arteries
What are the causes for poor
blood supply to the cord?
- Trauma
- Rupture of aortic aneurysm
- Dissection of the aorta
- Inflammation of aorta—vasculitis, collagen disorders
- Venous hypertension
- Degenerative spinal diseases and disc herniation
- Severe atherosclerosis and luminal narrowing
- Iatrogenic
• Vasoconstrictors in epidural space
• Surgical cross clamping of the aorta
• Coeliac plexus block
• Deliberate/accidental hypotension
What is AsA syndrome? What are the findings?
○ ASA syndrome—problems in the anterior spinal artery territory resulting in
critical ischaemia of the anterior part of the spinal cord.
○ The characteristic findings are
Motor
• Loss of motor function bilaterally below the level of lesion due to the
involvement of corticospinal tracts
Sensory
• Loss of spinothalamic tracts resulting in bilateral thermoanaesthesia
• But intact light touch, vibration, and proprioception due to preservation of
posterior columns
Autonomic
• Sexual dysfunction; loss of bladder and bowel function due to the effect on
descending autonomic tract
See Figure 2.9.
A 78-year-old female is booked for bunion operation. She complains
of chest pain on her right side, cough, and weight loss.
How do you preassess her?
History
• Anaesthetic history, paying particular attention to cardiac and respiratory function
• Smoking history
examination
• Signs of weight loss and cachexia
• Cardiovascular and respiratory examination
investigations
• Routine bloods, cross matching
• Arterial blood gas
• Lung Spirometry, diffusion capacity (DLCO), predicted postoperative FEV1
• Cardiopulmonary exercise testing (CPET)
What is DLco, and how do you measure it?
DLCo is the diffusion capacity and is calculated by measurement of carbon monoxide taken up by p
What values of the lung function tests would you accept before proceeding to surgery?
○ The flow chart in Figure 2.5 is an amalgamation of the British Thoracic
Society and American College of Chest Physicians’ guidelines.
○ The initial screening tool is of preoperative measured FEV1 with >2 litre
required for pneumonectomy and >1.5 litre for lobectomy.
○ If there is no diffuse lung disease and no comorbidity, achievement of the appropriate lung volume is sufficient.
○ When these threshold lung volumes are not present, full respiratory function testing allows calculation of the predicted postoperative FEV1 and DLCo.
○ If both are >40% and the oxygen saturation is >90% on air, the patient
is in an average risk group. If either (or both) the predicted postoperative
FEV1 or DLCo are <40%, the patient should undergo formal CPET.
○ The threshold Vo2 max of 15 ml/kg/min delineates between high- and medium-risk patients.
○ This patient is undergoing a thoracotomy and lung resection.
Describe soda lime in detail
○ Soda lime consists of 94% calcium hydroxide, 5% sodium hydroxide,
and a small amount of potassium hydroxide (0.1%) and silica to prevent
disintegration.
○ A dye or colour indicator such as ethyl violet is also added, which changes the colour when the soda lime is exhausted.
- This happens at pH < 10.
pH 13.5
○ Moisture content 14%–19%
○ 1 kg absorbs 120 L of carbon dioxide
○ When exhaled gases reach the canister, carbon dioxide absorption takes
place and heat and water are produced. The warmed and humidified gas
rejoins the fresh gas flow (FGF).
○ In a patient with tidal ventilation of 6 L/min and Co2 production of 250 ml/min, the soda lime will be exhausted in 6 hours at FGF of 1 L/min and in 8 hours if the FGF is 3 L/min.
What is the chemical reaction during the absorption of co2 by soda lime?
Co2 + H2o H2Co3
then
H2Co3 + 2 KoH - K2Co3 + 2 H2o + Energy
then
K2Co3 + Ca(oH)2 - CaCo3 + 2KoH
oR
Co2 + 2NaoH Na2Co3 + H2o + heat
then
Na2Co3 + Ca(oH)2 CaCo3 + 2NaoH
Each mole of Co2 (44 g) reacted produces one mole of water (18 g).
The overall reaction is
Ca(oH)2 + Co2 CaCo3 + H2o + heat
