Anaesthetics Flashcards
What is the ASA grading system?
Grade I; normal healthy patients, non smoker, no/ minimal alcohol intake
Grade II; mild systemic disease such as well controlled diabetes or hypertension, current smoker, obesity (BMI; 30-40), mild ling disease
Grade III; severe systemic illness such as poorly controlled diabetes/ hypertension/ COPD. morbid obesity (>40), history of ACS/ stroke/ TIA >3 months ago
Grade IV; severe systemic illness that is a constant threat to life e.g MI/ stroke/ severe valve problems, TIA within 3 months, sepsis, severely reduction in ejection fraction
Grade V; moribund patients not expected to survive operation such as ruptured abdominal aortic aneurysm, massive bleed, intracranial haemorrhage with mass effect
Grade VI; patient is declared brain dead and whose organs are being removed for
Causes of airway compramise?
Anaphylaxis
Thermal injury
Neck haematoma
Wheeze
Surgical emphysema
Reduced consciousness
Simple airway manoeuvres?
Suction; if visible blood, vomit, secretions or foreign body
Turn patient onto side
Head tilt and chin lift
Jaw thrust
Hook both fingers under the angle of the jaw and lift mandible forwards
Airway adjunct options?
Oropharyngeal airway; Guedel
Rigid plastic tube
Nasopharyngeal airway
Flexible rubber tube
Suppraglottic airway;
Laryngeal mask airway
i-Gel
Endotracheal tube
Surgical airway;
Tracheostomy
Cricothyroidotomy
Causes of C-spine injury?
Motor vehicle collisions
Falls from height
Diving accidents
Sports-related injuries, particularly contact sports and high-velocity sports
Direct impact to the head or neck
Acts of violence such as gunshot wounds or stabbings
Signs and symptoms of C-spine injury?
Neck pain
Decreased range of motion in the neck
Focal neurological deficits, such as weakness or numbness in the arms or legs
Signs of spinal shock, including flaccid paralysis and loss of bowel or bladder control
Differentials for C-spine injury?
Whiplash injury
Thoracic/ lumbar spine injury
MSK injuries
Traumatic brain injuries
What is the NEXUS critieria?
Used to identify low risk of C-spine injury, unlikely if the following are met;
Normal level of alertness
No evidence of intoxication
No painful distracting injuries
No focal neurological deficit
Absence of midline cervical tenderness
Investigations for C-spine injury?
History and examination
NEXUS criteria
CT spine
Management of C-spine injury?
Airway management
Semi-rigid collar
Secure heads with blocks and tape
How should signs of shock be investigated post operatively?
FBC
U+E
CRP
Cultures
What is a central line?
Catheter into large vein of neck, chest or groin used to administer fluids, obtain diagnostic tests, monitor specific medical conditions
Risk factors for central line complications?
Operator skill
Patient anatomy
Type and location of central line
Sterile technique
Duration of catheter placement
How are central line complications classified?
Mechanical
Infectious
Thrombotic
Examples of central line complications?
Air embolism
Bleeding
Pneumothorax
Infection
Phrenic nerve palsy
Medications which should be stopped prior to an operation?
Clopidogrel; 7 days
Warfarin; 5 days
LMWH; the night before
ACE-i; the day before
Short acting insulin preparation should be stopped the morning of the surgery
Sulphonylurea; held day of surgery
COCP; 4 weeks before
What is an epidural anaesthesia?
Injection of local anaesthetic into the epidural space around L3-L4 or L4-L5 vertebral level
Risks of epidural?
Maternal hypotension
Low pressure headache
Epidural haematoma
Monitoring after epidural anaesthesia?
Continuous CTG
Indications for fluid resuscitation?
Systolic BP <100mmHg
Heart rate >90bpm
Capillary refill >2s
Cool peripheries
Respiratory rate >20bpm
NEWS ≥5
Dry mucous membranes
Normal daily fluid requirements?
25-30mL/kg/day water
1mmol/kg/day sodium
1mmol/kg/day potassium
1mmol/kg/day chloride
50–100g/day glucose to limit ketosis
Basics of fluid resuscitation?
Identify cause of fluid deficit and respond appropriately
Fluid bolus of 500mL crystalloid over <15 minutes
Reassess using ABCDE approach
Further fluid boluses (up to 2000mL) may be required
What is lactic acidosis?
Commonest cause of metabolic acidosis due to raised lactic acid levels (>4mmol/L)
Aetiology of lactic acidosis?
Type A; tissue hypoxia
Hypoperfusion
Cardiogenic shock e.g. left ventricular failure
Hypovolaemia
Sepsis
Regional ischaemia (e.g. limb or mesenteric ischaemia)
Gangrene
Cardiac arrest
Hypoxaemia
Respiratory failure
Severe anaemia
Carbon monoxide poisoning
Methaemoglobinaemia
Increased oxygen demand
Seizures
Strenuous exercise
Type B; No tissue hypoxia
Type B1 - underlying disease
Liver failure
Malignancy
Renal failure
Thiamine deficiency
Diabetic ketoacidosis (DKA)
Type B2 - drugs or toxins
Salicylates
Paracetamol
Beta-agonists (e.g. salbutamol)
Propofol
Metformin
Antiretrovirals (e.g. zidovudine)
Alcohols (e.g. ethanol, methanol, ethylene glycol)
Cyanide
Type B3 - congenital metabolic defects
Mitochondrial disorders
Glycogen storage disorders
Primary lactic acidoses (e.g. pyruvate dehydrogenase deficiency)
Organic acidaemia (e.g. maple syrup urine disease)
Symptoms of lactic acidosis?
Hypotension
Tachycardia
Confusion
Prolonged capillary refill time
Cool peripheries
Oliguria
Signs of lactic acidosis?
Tachypnoea
Kussmaul’s breathing
Differentials for lactic acidosis?
Ketoacidosis
Uraemia
Drugs; salicylates, iron, metformin, isoniazid, ciclosporin
Poisoning; methanol, ethylene glycol, sulphur
Management for lactic acidosis?
Treat underlying cause
A to E approach
Supplementary O2
IV fluid resuscitation
Monitor urine output
Complications of lactic acidosis?
Hypotension (secondary to both vasodilation and myocardial depression)
Arrhythmias
Coma
Seizures
What is local anaesthetic toxicity?
When systemic levels of local anaesthetic exceed the maximum safe dose leading to bloackade of sodium ion channels disrupting neuronal function
What is the maximum safe dose of lidocaine?
3mg/ kg
Signs and symptoms of local anaesthetic toxicity?
Numbness or tingling around the mouth
Restlessness/agitation
Tinnitus
Shivering
Vertigo/dizziness
Subtle tremors of the face and extremities
Hypertension
Tachycardia
Decreased consciousness
Respiratory depression
Hypotension
Apnoea
Seizures
Sinus bradycardia
Ventricular arrhythmias
Asystole
Differentials for local anaesthetic toxicity?
Hyperventilation syndrome
Panic attack
Seizures
Cardiac arrhythmia
Investigations for local anaesthetic toxicity?
Observations monitoring
ECG
Management of local anaesthetic toxicity?
Stop drug
Continuous ECG monitoring
Lipid emulsion- 20% intralipid at a dose of 1mL/ kg every 3 minutes followed by infusion of 0.25ml/kg/min
What is malignant hyperthermia?
Life threatening crisis triggered by exposure to volatile inhalation anaesthetics or suxamethonium
Epidemiology of malignant hyperthermia?
More common in younger males, possibly due to higher rates of surgery
Aetiology of malignant hyperthermia?
Autosomal dominant mutation in ryanodine receptor 1 gene
Resulting in abnormal calcium regulation within muscles leading to increased calcium in sarcoplasmic reticulum
Signs and symptoms of malignant hypertermia?
Rapid increase in body temperature
Muscle rigidity
Metabolic acidosis
Tachycardia
Increased exhaled carbon dioxide
Differentials for malignant hyperthermia?
Neuroleptic malignant syndrome
Serotonin syndrome
Sepsis
Investigations to diagnose malignant hyperthermia?
Blood gas; metabolic acidosis, increased creatinine kinase
Temperature
Management of malignant hyperthermia?
Discontinue trigger
IV dantrolene
Restore temperature; ice pack, cool IV fluids, cooling blanket
Correct acidosis and electrolyte abnormality
How can position of NG tube be confirmed?
Measure pH of NG tube aspirate
Erect chest X-ray
What is CPAP?
Used in type 1 respiratory failure
Provides positive pressure to keep alveoli open for a longer period of time to facilitate gas exchange
What is BiPAP?
Used in type II respiratory failure with two different levels of positive pressure on inspiration and expiration
Criteria to start NIV?
Patient awake and able to protect airway
Co-operative patient
Consideration of quality of life of patient
Contraindications to NIV?
Facial burns
Vomiting
Untreated pneumothorax
Severe co-morbidities
Haemodynamically unstable
Patient refusal
Pre-operative management options of anaemia?
Oral iron if >6 weeks until planned surgery
IV iron if <6 weeks until planned surgery
B12/folate replacement
Erythropoiesis‐stimulating agent (ESA) therapy
Transfusion if profound anaemia and surgery cannot be delayed
Post operative management options of anaemia?
Transfusion
IV iron
Oral iron
Peri-operative management of steroids for patients who require long term therapy?
Switch oral steroids to 50-100mg IV hydrocortisone.
If there is associated hypotension then fludrocortisone can be added.
For minor operations oral prednisolone can be restarted immediately post-operatively. If the surgery is major then they may require IV hydrocortisone for up to 72 hours post-op.
Complications of poor peri-operative management of diabetes?
Hyperglycaemia
Hypoglycaemia
DKA
Lactic acidosis
Rules for hypoglycaemia agents on day of surgery?
Metformin (taken once daily) Take during the morning of surgery
DDP-IV inhibitors Take during the morning of surgery
GLP-1 analogues Take during the morning of surgery
SGLT-2 inhibitors Omit the day of surgery due to the risk of DKA
Insulin
Schedule the patient as early on the theatre list as possible, minimising the amount of time the patient is nil by mouth.
If on long-acting insulin, this should be continued but reduced by 20%.
Stop any other insulin and begin sliding scale insulin infusion from when the patient is placed nil by mouth.
Continue infusion until the patient is able to eat post-operatively.
Switch to the normal insulin regimen around their first meal.
Causes of post operative N+V?
Infection
Hypovolaemia
Pain
Paralytic ileus
Drugs
Management of post operative nausea and vomiting?
Non pharmacological; minimise patient movement, analgesia, IV fluids
Pharmacological;
5HT3 receptor antagonist; ondansetron
H1 receptor antagonist; cyclizine
D2 receptor antagonist; prochlorperazine
Dexamethasone
Metoclopramide
What is a poor urine output post operatively?
Decreased urine volume output after surgical procedure, less than 0.5ml/kg/ hour
Causes of post operative poor urine output?
Pre-renal: This results from decreased blood flow to the kidneys.
Hypovolaemia
Hypotension
Dehydration
Renal: This is due to intrinsic damage to the kidney tissues.
Acute tubular necrosis
Post-renal: This occurs due to obstructions that prevent urine from being expelled from the body.
Benign prostatic hypertrophy
Effects of drugs such as anticholinergic or alpha adrenoreceptor antagonists, often used in anaesthetics
Pain following surgery, particularly hernia operations
Psychological inhibition
Opiate analgesia
Signs and symptoms of poor urine output?
Decreased frequency or volume of urination
Hypotension and tachycardia (pre-renal causes)
Abdominal pain or discomfort, particularly after hernia operations (post-renal causes)
Symptoms of drug side effects such as dry mouth, blurred vision, and constipation (post-renal causes due to anticholinergic drugs)
Investigations to identify cause of poor urine output?
Urine output measurement
Urinalysis
Blood; U+E
USS KUB
Management of poor urine output?
Correct fluid an electrolyte imbalance
Manage underlying cause
Urinary catheterisation
Rules for pre-operative fasting?
Clear fluids upto 2 hours pre-op, includes water, fruit juice, coffee/ tea without milk
IV fluids
Last meal should be 6 hours pre-op
What is rapid sequence induction?
Coordinating the administration of rapidly acting induction agents to produce anaesthesia and muscle relaxation, followed by prompt intubation, securing airway with minimal risk of aspiration
Roles in RSI;
Airway
Drug preparation
Monitoring of vital signs
Drug administration
Cricoid pressure
Sequence of rapid sequence induction?
Preparation
Involves ensuring the environment is optimised, equipment is available and staff are ready
Preoxygenation
Involves the administration of high flow oxygen for 5 minutes prior to the procedure
Pretreatment
May involve administration of opiate analgesia or a fluid bolus to counteract the hypotensive effect of anaesthesia
Paralysis
The administration of the induction agent (e.g. Propofol or Sodium Thiopentone) and paralysing agent (e.g. Suxamethonium or Rocuronium)
Protection and positioning
Cricoid pressure should be applied to protect the airway following paralysis. In line stabilisation may be required in some cases.
Placement and proof
Intubation is performed via laryngoscopy, with proof obtained (direct vision, end-tidal CO2, bilateral auscultation)
Post-intubation management
Taping or tying the endotracheal tube, initiating mechanical ventilation and sedation agents
What is suxamethonium apnoea?
Defect in plasma cholinesterase enzyme required to metabolise suxamethonium resulting in a prolonged period of paralysis
Signs and symptoms of suxamethonium apnoea?
Prolonged paralysis following administration
Little/ no effort to cough or breathe spontaneously
Differentials for suxamethonium apnoea?
Myastensia gravis
Botulism
Poliomyelitis
Management of suxaethonium apnoea?
Intubation and ventilation until they can breathe on their own
Avoid use of suxamethonium in future
What is SIRS?
Systemic inflammatory response syndrome diagnosed if one or more of the following is present
Temperature >38 or <36 degrees Centigrade
Heart rate >90
Respiratory rate >20
White cell count >12 or <4 x10^9/L
Causes of major trauma?
Road traffic accidents
Falls (considered a dangerous mechanism of injury if height greater than 1 metre or 5 steps)
Assault (including non-accidental injury in babies and children)
Sports injuries
Accidents at work
Classification of TBI?
Based on GCS;
Mild - GCS 14-15
Moderate - GCS 9-13
Severe - GCS 3-8
