Critical Care Qs

Question 1

Post - Op Colectomy

Tachycardic and Unwell

i) Differentials
ii) Investigation of choice for PE

Answer 1

i) Differentials

Anastamotic leak, VTE, ARDS, Infection

Late- Wound Infection, Post-operative collection,

ii) CTPA - look for filling defect in the pulmonary arteries

Question 2

Trauma Patient - LOC + Vomiting + Concomitant ankle fracture

GCS subsequently Drops

i) Points of contact
ii) Possible CT Head findings
iii) Early CT Head Criteria

Answer 2

i) Contact - Anaesthetist/ITU, Neurosurgeons, Radiology, Senior Support
ii) CT Head findings - EDH, SDH, Contusion, DAI
iii) Canadian CT Head Rules - High 2, >65 years, basal skull fracture signs Intermediate - Dangerous mechanism, Retrograde amnesia

Consider arbitrary ct if - GCS <13, young patient, bleeding diathesis

Question 3

Raised ICP

i) What is the monroe kelly doctrine?
ii) Normal ICP/MAP/CPP
iii) How to measure ICP?
iv) Causes of raised ICP
v) Signs
vi) management
vii) Regulation of cerebral blood flow?

Answer 3

i) Monroe Kelly Doctrine centres around that there are three constituents in the brain - parenchyma, CSF and Blood. As the brain is contained inside a closed vault (skull) if any one of the constituents increases the others become displaced/the ICP rises.

ii) ICP - <25 (5-15) mmHg CPP - >65mmHg MAP - 90mmHg

iii) MAP - ICP = CPP

Need ICP monitoring + MAP monitoring to accurately gauge the CPP

Invasive MEasurement via - IVD, EVD (parenchymal, subarcachnoid, epidural)

Non invasive measurement via - Doppler, CT, Introcular pressure

iv) Causes - SOL, Bleed, Blockage in CSF drainage or decreased resorption/increased production/ cerebral oedema, obstructed venous outflow
v) signs - CN palsies, Cushings Triad (bradycardia, low RR + hypertension), pappilodoema
vi) management - Head up, normocapnea, IV mannitol, sedation, oxygenation, targeted BP management
vii) Cerebral Blood Flow:

Autoregulation between 50-150mmHg Systolic Pressure by myogenic stretch reflex in vessels

Low O2/ Low CO2 leads to Vasodilation

Question 4

Burns:

i) How to manage airway and breathing?
ii) Calculating percentage area of burns
iii) Calculating fluid requirement?
iv) type of fluid?
v) RFs for Smoke Inhalation Injury

Answer 4

Burns should be managed in a specialist burns unit and some patients will need ITU management (multi organ failure)

i) - High index of suspicion for inhalation injuries - These patients need early intubation as intubation becomes more difficult with time

Escharotomy if required for circumferential thoracic burns

ARDS is associated with burns

Suspect Carbon Monoxide poisoning

Ix -Serial ABGs, CXR, Capnography, Laryngoscopy

ii) Wallace Rule of 9s

Head + Neck - 9

Arm - 9 each

Chest/Upper back - 9 each

Abdomen / Lower back - 9 each

Leg -18 each

(Lund and Browder Chart is more accurate)

iii)Fluid requirement ( if >15% affected)

Parkland’s Formula - 4 x body weight x percentage burn.

1/2 in 8 hours 1/2 in 16 hours

(There is also a mount vernon formula)

iv) Fluid type

Crystalloid - prefered Hartmann’s to prevent hyperchloraemic acidosis

v) HO Fire in enclosed space, Soot around nostrils, Carbon sputum, singed nasal hairs, hoarse, Upper airway sounds, Drooling, COHb - >10

Question 5

i) Which nutrition sources in critical patients?

ii) What percentage of enteral feeding target in sick patients?

iii) Early parenteral feeding?

iv) Feedin in malnutritioned criticlaly ill patients

Answer 5

i) Carbohydrates are favourable. Protein is indeterminate - currently thought that critically ill patients have higher protein requirements. Fats thought to not be metabolised well in sick state.

ii) <30%. Agressive nutritional treatment was shown in trials to be associated with increased mortality

iii) Early parenteral feeding is associated with increased HAIs

iv) Traditionally patients who have moderate starvation have been treated with enteral/parenteral feeding as appropriate however mortality/hospital stay date have not validated these observations

Question 6

Criteria for malnutrition

Answer 6

i) Bmi <18.5
2) Weight loss of 2.3kg/ 5% in 1 month
3) Weight loss of 4.5kg/10% in 6 months

Question 7

Contraindications to enteral feeding?

Answer 7

i) Severe haemodynamic instability
2) Bowel Obstruction
3) Ileus (severe/protracted)
4) Major UGI bleeding
5) Prolonged vomiting/diarrhoea
6) GI Ischaemia
7) High output fistula

Question 8

Contraindicatiosn to parenteral nutrition?

Answer 8

i) Hyperosmolarity
ii) Severe hyperglycaemia
iii) Volume overload
iv) Poor IV access

Question 9

Feeding Calculations

i) in normal weight/ underweight

iii) obese patients

Answer 9

i) Initially 8-10 kcal/kg —> 18-25 kcal/kg in the first week and this can be increased in subsequent weeks
ii) Penn State University Prediction

Dosing Weight = IBW + 0.4(ABW-IBW)

Then with the dosing weight use the same kcal/kg parameters

Question 10

i) Types of delivery

ii) Basic components of feed)

iii) Normal or concentrated feed in CCI patients?

iv) Complications of PEG/PEJ

v) Complications of Nasoenteric tubes

vi) Contraindications to nasoenteric tubes

Answer 10

i) Pyloric:

NG Tube or PEG Tube

Post-pyloric (Gastric dysmotility, Gastric outflow obstruction, duodenal obstruction, oesophageal injury):

ND/NJ tube or PEJ Tube

ii) Feed Components

Isotonic,

1kcal/ml (can be more concentrated)

Protein - 40g/L (can be nonhydrolyzed protein)

Long chain fatty acids

Vitamins, nutrients + minerals

Simple and complex carbs

iii)

CCI patients usually given concentrated feeds yet lack of supportive evidence

iv) General - Tube dysfunction, Wound Infection, Nec Fasc, bleeding, leakage, ulceration, gastric outlet obstruction, removal, peritonitis,

Early - Pneumoeritoneum, ileus, visceral perforation,

Late - Deterioration of site, buried bumper syndrome (tight tube), fistulation, seeding along PEG tract,

v) Placement - pulmonary, Kinking/coiling

Nasal ulceration/necrosis

Visceral perforation

Increased risk of reflux due to sphincter dysfunction

vi ) Oesophageal stricture, oesophageal varices, base of skull fractures + bleeding risk

Question 11

i) Complications Enteral

ii) Complications Parenteral

Answer 11

i) Complications

Aspiration,

Diarrhoea (can be helped with fiber feeds),

Metabolic - refeeding syndrome, hyperglycaemia, nutrient deficienceis

Hypovolaemia

Constipation

High residual volumes
Nausea/Vomiting

ii) Line Related - Damage to structures, Thrombosis related to feed viscosity

Feed Related - Electrolyte, TGs, Glucose (High/Low), Thrombosis

Expensive , Gut atrophy, increased acute phase response

Question 12

ARDS

1) Causes
2) Features
3) Pathology
4) Management

Answer 12

Causes: Trauma, Sepsis, Pancreatitis, Cardiac operations, Pneumonia, Burns, TRALI, Drugs

Features:

Dyspnoea

Hypoxaemia despite high FiO2 (Early alkalosis on ABG then acidosis w/ tiredness)

CXR - Diffuse bilateral alveolar infiltrates

Decreased Lung Compliance

Absence of pulmonary oedema (Pul. Wedge. Pressure <20, absence of clinical signs of fluid overload)

Pathology:

Early - Exudative phase (oedema, inflammation, hyaline membrane formation)

Late - Development of fibroplasts, Collagen Deposition

Resolution - Fibrosis

Management:

Supportive: Sedation ( reduce oxygen requirement), Analgaesia, PPI, VTE Prophylaxis, Steroids (severe ARDS)

Oxygenaton:

FiO2 - generally high requirement but goal is PaO2 of 55-80, Prone positioning, ECMO,

Generally require invasive ventilation, Low tidal volume ventilation (mitigates alveolar injuries)

Question 13

i) Constituents

ii) Pulse deficit?

Answer 13

i) Cardiac Output = HR x SV (SV = End Diastolic Volume - End Systolic Volume)
ii) Pulse Deficit - Difference between palpated pulses and heart beats. Some pulse pressures may not be significant enough to generate a radial pulse esp. as seen in arrhythmias.

Question 14

1) Intitial Stabilisation
2) Type 2 RF
3) Initial Management
4) Initial Imaging

Answer 14

1) NEXUS Clearance (low risk) - if none of the following present then CT C Spine can be avoided:

i) Focal Neurology, ii) spinal tenderness, iii) altered consciousness iv) distracting injury v) intoxication

If high risk mechanism (or significant intracranial trauma/pevlic trauma/neurological sx) - Immobilisation with C Spine Collar and blocks. Some centres use a spinal board.

2) T2RF - i) Think Cord Injury/spinal shock (apraxia) ii) phrenic nerve injury iii) Think Head injury iv) Obstruction to airway

C3 and above - Immediate resp. paralysis

Below - delayed phrenic nerve palsy

3) Initial Management:

After in line stabilisation.

Hypoxaemia - Supplemental oxygenation with some mechanical ventilation. May need early intubation (and later on trachy placement)

Hypotension - Due to other injury/ spinal shock - Legs up, IV therapy + ?Pressor Support

Bradycardia - Consider Atropine

Urinary Retention - may need catheter insertion

medical - PPIs, Steroids,

4) A-P X Ray + Lateral (Need to be able to see up to T1).

Swimmer’s View - helpful to view C7/T1. Aim is to anteriroly displace the humeral hads

Question 15

1) Types of shock
2) BP components
3) Shock Categories

Answer 15

1) Types: Distributive (Septic, SIRS, Inflammatory) , Hypovolaemic, Neurogenic, Cardiogenic, Obstructive (pulmonary)

2) BP Components - CO x Systemic Vascular Res.
3) Categories

I (<750ml/15% loss) - no features

II (750ml-1.5L/ 15-30% loss) - Signs, HR >100, RR>20, UO 20-30ml

III (1.5l-2L/30-40% loss) - Signs, HR>120, RR> 30, UO 10-20ml

IV (>2L/>40% Loss) - Signs, HR >140, RR>40, UO <10

Question 16

What to say in the case of a septic patient?

Answer 16

1 - A-E Approach

2 - Meets SIRS criteria

3 - Management:

Early Goal-Directed Therapy with Circulatory Optomisation

• Which setting can she be managed in?
• Urine output, Cardiac Output, CVP Monitoring

Early Goal-Directed Therapy with Circulatory Optomisation is:

• when lactate >4 –> 20 ml/kg crystalloid minimum as an initial resuccitation measure
• Where the initial resuscitation measure does not work –> Vasopressors to aim for MAP >65 mmHG / CVP >8mmHg/ Central Venous Oxygen Sats >70%

Question 17

i) Bloods for patient with abdominal pain + SIRS

ii) Imaging for same clinical scenario

Answer 17

i) FBC, U+E, CRP, LFT (+GGT, ALT, AST), Clotting, Blood Cultures

Pancreatitis: LDH, Albumin, Lab GLucose, Amylase, Lipase, ABG

Group + Save

ii) Erect Chest XR

USS Abdo

CT (if no cause found)

Question 18

Scoring Systems for Pancreatitis:

Answer 18

i) Modified Glasgow Criteria (>3 = Severe and should be escalted to intensive care team):

Pao2 <8

• *Age** >55
• *Neutrophils** >15
• *Calcium** <2.0
• *Renal** Urea >16
• *Enyzmes** LDH>600/ AST>100
• *Albumin** <32

Sugar >10

Ranson Criteria

Balthazar CT Scoring

APACHE II

Note CRP >140 confers poor prognosis

Question 19

i) Potential Complications of Panreatitis

ii) What is a pancreatic pseudocyst

iii) Complications of chronic pancreatitis

Answer 19

i) Early

Local - Necrotising Pancreatitis, Superimposed Infection, Paralytic Ileus, Haemorrhage Pancreatitis

Systemic - SIRS, ARDS, Hypocalcaemia, Pleural effusion (Left), Hypovolaemic Shock

Late

Local - Pseudocyst, SMV/SV/SMA/SA thrombosis/heamorrhage, Intrabdominal Collection

ii) Pancreatic Pseudocyst - encapsulated fluid collection encased within a fibrous capsule

1/2 -Resolve spontaneously 1/2 - Require drainage (IR/Endoscopic/ Open)

iii) Malnutrition (Lipase,Proteinase Deficiency)

Osteoporosis

Chronic pain

Diabetes

Structural - Collections, Fistulation, Biliary Obstruction(strictures), Abscess

Question 20

Pancreas Function

Answer 20

Endocrine:

B Cells - Insulin

Alpha Cells - Glucagon

D Cells - Somatostatin

PP Cells - Panceratic Polypeptide

Exocrine: (activated by CCK)

Proteins- Trypsinogen - activated by enterokinase –> Trypsin

Lipase - Fats

Amylase - Carbs

Alkaline - Neutralises stomach acid

Question 21

Acid Base

i) What is the Henderson-Hesselbach Equation?

ii) What is chloride shift?

iii) Normal Anion Gap? Causes of normal/High anion gap acidosis

iv) Causes of metabolic alkalosis

v) Causes of Respiratory Acidosis?

vi) Causes of respiratory alkalosis?

Answer 21

i) HCO2 + H+ –> HCO3- + CO2
ii) Chloride Shift:

Process by which RBCs can exchange Chloride Ions for Bicarbonate Ions.

Pulmonary Blood: More H+ than CO2. So RBCs produce H2O+ CO2 leading to less HCO3- in RBCs. Therefore Chloride ions move out of RBCs and HCO3- moves in

Systemic Blood: More CO2 than H+. So RBCs produce HCO3- + H+. THis leads to HCO3- moving out of RBCs and Chloride ions moving in.

iii) Anion Gap: 10-14

Normal - RTA, Tubular Damage, Loss of HCO3- (intestinal), Hyperparathyroidism, Hypoaldosteronism (RTA IV)

High - Lactate, Methanol, Hyperkalaemia, Salicylates

iv) Metabolic Alkalosis - H+ Loss (Vomiting/ Renal), Hypochloraemia, Diuretics, Antacids

v) Airway Obstruction - Asthma/COPD,

Altered gas diffusion - pneumonia, ARDS, oedema

Central Causes - Head Inj, Myaesthenic, Drugs, flail segment, polio

vi) Respiratory Alkalosis - Hyperventilation, Saliclylate, Pulmonary Embolus

Question 22

i) DDx for a cool/painful leg

ii) Causes of embolus

iii) Where do emboli tend to get stuck?

iv) Investigations for ALI?

Answer 22

i) Acute on Chronic, Acute embolic, Vascular injury, Venous Thrombosis, Neurological

ii) Embolus:

AF/Cardiac Thrombus, Proximal Aneursym, Atherosclerotic Plaques

iii) Emboli tend to get stuck at bifurcations

iv) If evidence for emboli is clear argument for immediate embolectomy without imaging.

If the event may be thrombotic useful to have Angiography CT beforehand to plan procedure

Investivation choice also depends on clinical severity - If muscular paralysis the limb is non salvageable. If Paraesthesia - urgent revascularisation is necessary. If approaching 6 hour mark consider urgent intervention

Question 23

Acute Assessment of Sick Patient (CCRISP)

Answer 23

A - Assess airway. If concerns of compromise assess further - with look listen and feel approach:

• Attempt Suction
• Airway Adjuncts
• Oxygen

B - SaO2/ABG

Chest Exam - tracheal deviation, Good air entry, any added sounds, good expansion

C - IV Access + Bloods, ECG, Cardiac Monitoring (Incl BP)

Fluid Assessment - JVP, CRT (central+peripheral), Heart Rate, Ausculate chest, Look for oedema

D - Pupils, Glucose, Neurological status (GCS/ AVPU)

E - Expose and full examination

Question 24

Acute Limb Ischaemia Classification

Answer 24

I + IIa - May have time for imaging

IIb + III - Probably not time for imaging

Question 25

What consitutes SIRS:

Answer 25

2 or more of:

Temp >38 / <36

RR >20 / PaCO2 <4.3

Pulse >90

WCC > 11 / <4

Question 26

Define:

i) Acute Renal Failure

ii) Timeframe to develop acute renal failure

iii) Causes of renal failure

iv) Causes of ATN (main 2)

v) Investigations for Acute Renal Failure (immediate)

vi) Basic Management (+ if there is concomitant pulmonary oedema)

vii) Oliguria

Answer 26

i) An acute accumulation of toxic metabolites due to impaired renal excretion
ii) Over the course of 48 hours
iii) Pre Renal - Hypovolaemia, Shock States, Renal Artery Stenosis

Renal - ATN, Glomerulonephritis, Interstitial nephritis, Hepatic Renal Syndrome

Post Renal - Urinary Tract obstruction (ureters, bladder, Urethral), Abdominal Compartment Syndrome

iv) ATN - Ischamic Hit (renal hypoperfusion), Nephrotoxins (Aminoglycosides, Tetracyclines, Paracetamol, Myoglobin, Myeloma, Heavy Metals)
v) Urine Dip, MC&S, LFTs (HRS), ABG (Lactate), CRP, Bone Profile (?High Ca++)

Not first line - US KUB/CT KUB, ACR/PCR, Renal Screen (myeloma, autoimmune)

vi) Treat precipitant!

Then - Stop nephrotoxins, Input/Output Monitoring (Cathter/CVP pressure monitoring .UO 0.5 ml/kg/hour in Adult, 1 ml/kg/hour in Child) , IV Fluid Provision (20-30 ml kg day is maintenace so if under filled will need more than this)

Pul. Oed. -

Sit patient up - oxygenate. CXR. ABG.

No fluids. IV Furosemide (If SBP <100 then can try GTN infusion) . Strict input/output monitoring

vii) Oliguria - <400 ml urine output per day

Question 27

Hypoxic Patient:

i) Initial Investigations
ii) Define ARDS
iii) Causes of ARDS

iv ) Management of ARDS

v) Mortality

Answer 27

i) CXR, ABG, ECG, Fluid Balance Chart

Bloods - FBC, CRP, ?Troponin, Us + Es ?Pul. Oedema

CTPA - if high Well’s Score

ii) ARDS - Acute respiratory failure and non cardiogenic pulmonary oedema with reduced lung compliance + hypoxia . Often refractory to oxygen therapy.

All of these are required -

a) Normal/ Low Pulmonary Capillary Wedge Pressure (<18 mmHg)

b) Diffuse bilateral pulmonary infiltrates

c) PaO2/FiO2 Ratio - <26.6 kPA

iii) Causes -

Pulmonary - Pneumonia, PE, Aspiration, Fat embolus, Smoke ihalation, Trauma

Cardiac - Cardiothoracic Surgery

Systemic - Sepsis, Pancreatitis, Trauma, Massive Transfusion, DIC

iv) Management:

Oxygenation

Ventilation - Prone, Prolonged inspiration (reverse I:E ratio), High PEEP (risk of alveolar trauma)

Drugs - (no evidence) Prostacyclin, Steroid, NO

v) Mortality - 50-60%

With sepsis - 90%

Question 28

Present This

Answer 28

PID, Date, Time, PA/AP,

Diffuse Bilateral Pulmonary Infiltrates:

Suggestive of ARDS, Pulmonary Oedema, Pneumonitis, TRALI (If transfused recently)

Technical Adequacy Points:

Rotation - Equal distance between clavicles and spinous processes

Insipiration - 5 Anterior Ribs

Penetration - Vetebral bodies behind the heart should just be visible

Exposure - Costophrenic Angles + Apices included?

Question 29

AIrway:

i) Indications for surgical airway

ii) Location of cricothyroidotomy

iii) Location of tracheostomy

Answer 29

i) Indications for surgical airway - Failed intubation + Laryngeal Trauma

ii) Cricothyroidotomy - Through cricothyroid membrane/ligmanet

iii) Tracheostomy - Through the 2nd - 5th Tracheal Rings

Question 30

Which layers do you traverse when creating a tracheostomy?

Answer 30

Skin

Subcutaenous Fat

Fascia + Platysma

Investing layer of deep cervical fascia

Infrahyoid Strap Muscles (retracted)

Pretracheal Fascia

Thyroid Isthmus

Trachea

Question 31

i) Consequences of poor pain management

ii) Gross description of pain pathway

iii) Indications for PCA (another card somewhere too) - Dosing

Answer 31

i) Poor Patient Experience

Poor Mobility –> Incr. DVT risk and delayed recovery

Poor cough –> Incr. risk of HAP

Incr. Sympathetic tone –> Incr. myocardial oxygen demand, delays gastric emptyinh

ii) Noiciceptors

–> A Delta Fibers (Fast and sharp pain)

–> C Fibers (Slow and diffuse pain)

Both synapse in ipsilateral substantia gelatinosa

–> decussate and travel more ventrally up the spinal cord to synapse in the thalamus.

—> Through corona radiata to cerebral hemispheres

iii) Severely painful conditions + major surgery:

Purely bolus w/ time lockout period or

Basal Bolus administration

Dosing - 0.5mg-1.5mg Diamorphine with 3-5minute lock out period

Question 32

Risk factors for chronic post surgical pain

Answer 32

Pre operative pain

Chemotherapy

Long Surgery

Severe post operative pain

Question 33

Blood Transfusions:

i) Shelf life of blood products

ii) Infections screened for in blood

iii) Complications of transfusion

iv) What is a massive transfusion + Complications

v) Ratio of blood products in massive transfusion?

Answer 33

i) Blood - 35 Days (2-6 degrees)

Platelets - 5 Days (20 degrees)

Cryoprecipitate/FFP - 1 year (-30 degrees)

ii) Infections screened - HIV, Hep B +C, Sphyllis, HTLV

CMV - in FFP

iii) Immediate - Febrile Transfusion reactions, Haemolytic Transfusion Reactions, Anaphylaxis, Coagulopathy

Delayed - Delayed Haemolytic Transfusion Reaction, TRALI, Overload, Hyperkalaemia, Hypocalcaemia, Infection, GvHD, Post-transfusion purpura

iv) When 50% circulatory volume is given within 4 hours/ 100% circulatory volume in 24 hours. Complications are :

• Electrolyte disturbance(High K+, Low Ca++), ARDS/TRALI, Fluid overload, Coagulopathy, Hypothermia, Metabolic Alkalosis

v) 2:1:1 RBC:Platelets:FFP

Inter-trust variation.

Question 34

Alternatives to blood in Jehova’s Witness

Answer 34

Fluids

Pharmacology - Fe+, EPO, TXA, Factor VIIa

Blood - Autologous, Cell Saver

Intraoperative - Haemostasis, Monitoring and optomisation of homeostasis

Question 35

• *Brainstem Death:
  i) Reversible Causes of coma?**

ii) Who assesses for brainstem death?

iii) Examination?

iv) Absolute/Relative CIs to organ donation

Answer 35

i) Toxins - Lots of drugs

Hypothermia, Shock, Endocrine - thyroid, addison’s, glucose, Electrolyte- Na+, uraemia, ammonia

ii) 2 independent doctors at different times - 1 consultant and both >5 years experience . Neither should be involved with patients who have patients potentially receiving the organs.

iii) 5 things - Absent VOR, Fixed Pupils, Absent Corneal response, Absent motor responses to pain, Absent cough/gag reflex

Then - Apnoea Test:

Oxygenate to >95%

Decrease ventiltion rate to - ETCO2 >6.0 and confirm ABG CO2 >6.0 and pH <7.4

Then stop ventilation, continue oxygenation with 5L through ET

Observe 5 minutes. If ABG shows >0.5 rise in CO2 then confirmed loss of respiratory drive

iv) Absolute - vCJD + HIV

Relative - Liver failure, TB, Metastatic cancer and high age

Question 36

Types of ventilation

Answer 36

Supplementary - NC, Venturi, non re breathe, adjuncts

Non invasive - BiPAP, CPAP, Optiflow

Invasive - ET, Trachy

Question 37

Burns Classification

Answer 37

Question 38

i) Criteria for admission to specialist burns unit

ii) Particulars of Hydrofluoric Acid Burns

Answer 38

i) Area - >10%(Adult)/ >5%(child) Total SA

Location - Face, Flexural Surfaces, hands, feet and circumferential burns

Type - Steam, Electricity, Chemicals

Patient Specific - <5/>60 years old, Severe Comorbidities

ii) Hydrofluoric acid burns can be devestating:

Electrolytes (Hypocalcaemia, Hyperkalaemia, Hypomagnesaemia)

Necrosis including of the bone

Question 39

Central Line:

i) Indications

ii) Complications

iii) Insertion Guidelines

iv) IJV Surface Marking

v) Describe procedure - IJV + SCV

vI) Removal

Answer 39

i) Indications include - TPN, Drugs (amiodraone/K+), CVP monitoring, Transvenous Pacing, Haemodialysis, Failed IV access
ii) Complications include - Arterial Puncture, Pneumothorax, Air Embolus, Thrombosis, infection, Cardiac Arrhthmias, Atrial Perforation, Thoracic Duct Damage

iii) A) US GUidance B) X Ray to check - SVC Cannulated and no pneumothorax

iv) Apex of both SCMs (Lateral to Carotid)

v) IJV - Head Down. Turn head other way. US Guidance.

Palpate carotid and go lateral.

Seldinger Technique. Introduce needle at 30 degree angle pointing at the nipple. Keep aspirating and when you get blood advance catheter

SCV - Same technique except needle insertion at midpoint inferior to clavicle pointing towards suprasternal notch.

vi) Removed either flat/ head down - prevents air embolus

Check clotting plateleets before hand

Send tip for MC&S if concerns about infection

Question 40

Which layers do you pass through to insert a subclavian line?

Answer 40

Skin

Subcut Fat + Fascia

Pec Major

Subclavius Muscle

Subclavian Vein

Question 41

i) What is Frank-Starling’s Law?

ii) What would it imply if the curve of cardiac output x venous return shift to the right?

Answer 41

i) With increased Pre-Load ( Left Ventricular- End Diastolic Volume ) there is increased Stroke Volume:

Due to the effect of stretch on the ventricular wall leading to increased contractility.

ii) Indicates reduced contractility of the myocardium so reflects redued ability to cope with increased venous return and preload. inversely in exercise/fit hearts and reduced systemic resistance (afterload) left shift can be observed where contractility is increased

Question 42

i) Describe a CVP Trace

ii) Causes of increased/decreased CVP

Answer 42

i) Ascents - ACV

Descents - XY

a - atrial contraction

c- tricuspid closure (during isometric contraction of ventricles)

x - atrial relaxation

v - venous return to the atria

y - tricuspic valve opening

ii)

Decreased - Hypovolaemia, Vasodilation

Increased - Fluid Overload, Cardiac - Failure, Tamponade, Cor Pulmonale,

Question 43

Outline ATLS appraoch

Answer 43

Know resources available to you. Ask for monitoring to be attached including cardiac monitoring.

C - Hard Collar, Sandbags and tape until such time as the C Spine could be cleared using a tool such as the NEXUS criteria / Imaging

A - Airway assessment - talking? upper airway sounds? no breath on face?

Suction/Adjuncts/Tube/Surgical Airway

B - SaO2/ABG/RR

Examine - Expansion, Percussion + Auscultation

Emphysema/ Trachea position

Observe for any open chest/penetrating chest injuries/ asymmetrical chest movements

Attach Oxygen if indicated and start with highflow

C - 2 Large bore Cannulae - take bloods

BP/Cardiac Monitoring/ECG.

Central + Peripheral Pulse/ CRT / Skin mottling

Look for blood - Chest/ Abdo/ Long bones/ Pelvis/Floor

Warmed Crystalloid

D - PEARL/ GCS / Peripheral neurological examination

E - Environment assessment

Expose the patient and perform a log roll carefully

Urinary Catheter / NG Tube / Trauma Series (Chest, Pelvis, + C- Spine) / Low Res CT

Question 44

Describe

Answer 44

AP Radiograph of ? taken at ?

Communited mid-shaft tib / fib fracture with some varus displacement of distal fragments noted. Knee and Ankle appear to be intact however I would like:

Lateral Tib/ Fib and dedicated knee/hip/ankle films to be certain.

Risk of neurovascular compromise due to vascular/nervous/compartment syndrome is high so i would assess for these. Another risk would be rhabdomyolysis is this was a crush injury

Also be certain to not miss other injuries as this is likely to be a distracting injury

Question 45

i) Causes of rhabdomyolysis

ii) Lab Testing

iii) Complications

iv) Management

v) Myoglobin vs Haemoglobin in terms of oxygen dissociation

Answer 45

i) Crush Injury

Fracture

Burns

Hypothermia/Hyperthermia

Acute Limb Ischaemia

Connective Tissue Disorders/Haemophilias

ii) CK, Renal Function, Electrolytes, (High K+, High PO4-, Low Ca+), Blood Gas (pH, lactate), LDH, Urinary Casts (brown)

iii) AKI / Acute Renal Failure (ATN) + DIC

iv) Management:

Fluid Balance Monitoring (likely needs to be intensive)

May need haemodialysis to remove the toxins

Some extensive dialysers (high-flux) Can remove myoglobin (muscle oxygen binding protein) themselves

v) Myoglobin has a steeper dissociation curve as it only has 1 binding site for oxygen cf haemoglobin. Therefore at lower partial O2 pressures oxygen won’t dissociate allowing muscles to utilise oxygen in low/no oxygen environment.s

Question 46

WRT Compartment Syndrome:

i) Weak pulses/paraesthesia mean?

ii) What is compartment syndrome?

iii) Causes of compartment syndrome

iv) How to measure compartment pressure?

v) Management

Answer 46

i) Bad- Late signs.

Require urgent treatment at this point.

Pain out of proportion with clinical picture is the earlier sign of compartment syndrome.

ii) Compartment syndrome - is where the intracompartmental pressure exceeds capillary pressure thus reducing vascularisation of muscles/ nerves
iii) Causes - Fractures, Crush, Burns, Dressings, Extravasation injury, Postischaemic,
iv) Compartment pressure measurement probe/ Arterial Line

v) Keep limb at level of heart.

Release any pressure (Plaster)

Two incision four compartment debridement (either side of the tibia)

Question 47

i) What test of coagulation is most effected in liver damage / obstructive jaundice?

ii) Why does ALP rise in obstruction?

iii) Where is GGT found?

iv) WHat does bile do?

v) What is bilirubin precursor and how is unconjugated bilirubin transported to the liver?

vi) Is bilirubin reabsorbed?

vii) Correcting hepatic coagulopathy

Answer 47

i) Prothrombin Time (Measure of Extrinsic Pathway - I, II, V, VII, X):

This is because the liver is the site of production of the vitamin k dependent clotting factors (II, VII, IX, X), which tend to have short half lives.

In obstruction vitamin k absorption is impaired.

ii) ALP rises in obstruction as it is concentrated in the epithelial cells of biliary canuli. Disruption to this epithelium will therefore release ALP.

iii) GGT- Small Bile Ducts + Hepatocytes

iv) Bile - Emulsifies fats –> Fatty Acids –> Allows absorption of Vit ADEK

Bile is reabsorbed in distal ileum

v) Haem -> Biliverdin -> Bilirubin (Unconjugated -> Transported to liver on albumin –> Conjugated Bilirubin ( Glucoronyl Transferase )

vi) Bilirubin is converted to stercobilinogen -> stercobilin by oxidation in the bowel.

Some stercobilinogen is reabsorebd –> becomes urobilinogen in the liver -> urobilin

(answer is no)

vii) Vitamin K < FFP < PTCC

Question 48

i) Define: DIC

ii) Why is the D Dimer raised in DIC?

iii) List causes of DIC

Answer 48

i) A pathological consumptive coagulopathy whereby there is simultaneous activation of coagulation factors leading to fibrin deposition and fibrinolysis.

This leads to platelet and coagulation factor consumption.

Combined risks of microvascular thrombosis + severe bleeding risk

ii) D Dimer is raised as it is a breakdown product of fibrin. Due to enhanced fibrinolysis activity there is increased fibrin breakdown and increased D Dimer levels.

iii) Infectious - Any systemic infection

Malignancy - APML (M5)

Pregnancy- Abruption, Ecclampsia

Haematological - MAHA

Transfusion Reaction

Trauma - Burns, Polytrauma

Hepatic Failure

Question 49

Hypothermia:

i) Definition

ii) Consequences

iii) Intraoperative causes

Answer 49

i) <36 degrees

Mild - 35-32

Moderate - 32-28

Severe - 28-20

ii) Consequences:

Decreased Oxygen Dissociation from Hb - myocardial ischaemia, cerebral ichaemia, limb ischaemia, bowel ischaemia

Hypocalcaemia

Met. Acidosis

Arrhythmias

Coagulopathy - Enzyme Function impiarment + Platelet Dysfunction

Enzyme Dysfunction

Renal Failure

Pancreatitis

iii) Intraoperative Causes:

Preop hypothermia, Major Surgery, Long Surgery, Using GA + LA, Blood Loss/Transfusion

Question 50

EPidural:

i) Which Space/which layers do you go through?

ii) What could thoracic epidural do to respiration?

iii) What could a thoracic epidural do to the cardiovascular system?

iv) Consequences of high thoracic block

Answer 50

i) Between dura and ligamentum flavum ultimately.

Goes through - Skin, Subcut Fat, Fascia, Suprasinous Lig., Interspinous Lig., Ligamentum Flavum.

ii) It could paralyse the intercostal muscles at and below the level it is insreted at thus impairing chest wall expansion

iii) Distributive shock - cause vasodilation

Bradycardia - due to the drug cocktail used

T1-T5 level could impair the sympathetic stimulation to the heart thus preventing an appropriate rise in HR

Above C4- Respiratory Depression/ Arrest

iv) Hand paralysis, Respiratory Compromise (intercostal nerves), Cardiovascular compromise (cardiac sympathetics), Urinary Retention

Other complications:

Haemorrhage (Be careful when using antiplatelets/anticoagulants)

Question 51

Petechial rash over fat, neck and axillae

i) Features

ii) Causes

iii) Pathophysiology

iv) Mode of death

v) Test Results

vi) Mx

Answer 51

Fat Embolus Syndrome

i) Described by Bergmenn in 1873 as a triad:

Petechial Rash- a)Due to thrombocytopenia (purpura) and b) cutaneous vessel embolsiation

Respiratory Compromise - a) VQ Mismatch b) Capillary Permeability (due to inflammation) -> oedema c) Pneumonia

Cerebral Features - a) Microembolisation leading to hypoxia b) Lipase degradation of cerebrum

(Renal, Retina, Tachycardia, Pyrexia)

ii) Causes:

Traumatic - Long Bone Fractures/ Orthopaedic Procedures (reaming/ KR)/ Massive soft tissue injury

Atraumatic - Pancreatitis, Omental Fat Necrosis, BM transplant, Liposuction, Cardiopulmonary bypass, Sickle Cell,

iii) Patho:

Mechanical - Local ischaemia and tissue injury due to fat globule impaction in pulmonary and systemic vasculature

Biochemical - Catecholamines + Steroids –> activeate lipases –> break down fat to FFA which cause capillary permeability + lead to pul. damage

Coagulation - Thromboplastin from marrow –> activate coagulation/complement cascade –> intravascular coagulation

iv) Mode of death is usually right heart failure.

This is rare and only apparent with fulminant fat embolus syndrome (most severe of three clinical presentations)

v) ABG - Increased pulmonary shunt fraction

ECG - Tachycardic/ RHS

FBC - Low Hb, Low Plt,

CLotting - looks like DIC

Impaired renal function

Low Albumin Low Ca++

Urine and Sputum contain lipids

CXR - Pulmonary Infiltrates (fluffy snow storm appearance)

MRI- Multiple acute infarcts

vi) Prophylactic - Early Steroid Therapy, Ex-Fix device, Over-reaming femur in TKR, Decreased shaft width reamers, Early Fixation

Intensive Care Setting

Oxygenation/Ventilation - Early on CPAP

Albumin - Binds FFAs

Fluid Balance Monitoring (Invasive)

Correcting of electrolyte abnormalities

DVT prophylaxis

Question 52

i) Define : Fistula

ii) Define: Sinus

iii) Define: Abscess

Answer 52

i) A fistula is an abnormal connection between two endothelial/epithelial surfaces lined by granulation tissue

ii) A sinus is a blind ending tract lined by granulation tissue

iii) A localised collection of pus surrounded by granulation tissue

Question 53

Fistulae:

i) Causes of Enterocutaneous Fistula

ii) Classifying Fistulae

iii) Complications of high output fistulae

iv) Enterocutaneous Fistula Management

Answer 53

i) Abdominal Surgery (3/4)

Spontaneous (1/4):

• Inflammatory Conditions - Malignancy - Irradiation - Ischaemia

ii) a) Congenital/ Acquired b) Type - Enterovesicular, enterocolic, enterocutaneous, c) aetiological

d) Output:

Low- <200ml

Moderate - 200-500 ml

High - >500 ml

iii) Complications:

• Dehydration (Kidney Injury)
• Electrolyte Imbalances (HypoK+, HypoNa+, Acidosis)
• Malnutrition
• Infection - Abscess, cellulitis
• Intestinal Failure

iv) Initial Resuscitation with A-E

MDT approach - Surgeon, Dietitian, Stoma Nurse

SNAP

S epsis control

N utrintional Support (Initially TPN)

A natomical assessment / Adequate fluid/electrolyte management

P lan treatment / rotection of skin

60% Spontaneously resolve if - not infected/ adequate nutrition/ no distal obstruction

Surgery can be considered if :

Conservative management fails

Ongoing infectious concerns

Surgery aims to:

Excise Tract

Resect affected segment of bowel

Exteriorisation/anastamosis

Question 54

i) What prevents spontaneous healing of fistulae?

ii) Imaging modalities for fistulae

Answer 54

i) 60% Spontaneously Heal:

Otherwise causes are:

Distal Obstruction

Inflammatory Conditions / Sepsis

Malignancy

Foreign Body

Radiation

High Output

Malnutrition

ii) CT is Usually First Line but the best modality is a fistulogram (contrast being given through fistula outlet)

Anorectal fistulae - Endoanal ultrasound / MRI are other modalities considered

Question 55

i) Normal Calorific Requirements

ii) Calorific Requirements in extensive trauma patients

iii) Caveats in critically ill patients?

iv) Complications of TPN

Answer 55

i) 25-30 Kcal/kg/day

ii) 45-55 kcal/kg/kday

iii) In critically sick patients:

There is disparity in the practice that is performed. Some data suggests early agressive nutritional support is associated with increased mortality and early parenteral support is assocaited with increased HAI.

Generally a stepwise increase in calorific provision starting at less than <20 kcal/kg/day gradually increasing this.

iv) TPN Complications:

Related to Central Line Insertion

Electrolyte abnormalaties - HypoK+, Mg++, PO4-
Glucose high/low

TGs - High

Ess. Fat. Acid - Low

Question 56

Portal System:

i) normal pressure

ii) Sites of anastamosis with systemic system?

iii) What are oesophageal varices?

iv) Emergency Endoscopic Treatment Options for Varices? If Refractory to these?

Answer 56

i) <10 mmHg

ii) 6 - Lower oesophageous, Upper Rectum, Retroperiotoneum, Bare Area of the liver, Patent Ductus Venosus, Umbilicus

iii) Resultant from portal hypertension leading to venous engorgement of the oesophageal venous plexus (2/3 develop acute bleeding)

iv) a) Band Ligation b) Sclerotherapy –>

c) Sengstaken-Blakemore Tube (Baloon position need to be checked - Oesophagus & Cardia of stomach by X Ray before inflated) - can be complicated by oesophageal necrosis, perforation and aspiration pneumonia

Further d) TIPS (shunt between HV + PV)

e) Surgical Shunt f) Liver Transplant

g) Both Terlipressin (V1>V2 receptor agonist) + Octreotide ( Somatostatin analogue) Both cause splanchnic/portal vasoconstriction reducing blood flow flow to the varices + Prophylactic Antibiotics for all patients

h) Propranolol for prophylaxis

Question 57

i) What specifics do you look for when assessing head injury?

ii) Preventing secondary brain injury

Answer 57

i) Base of Skull/ Cribiform Plate injury - CSF Rhinorrhorea/Otorrhoea, Raccoon Eyes, Battle Sign

PEARL - Anisocoria/Absent VOR (if C Spine clear)/ Gaze Palsy

GCS

Neurological Exam - CN/ UL/ LL. Hoffman’s/ Babinski

ii) 1. Rapid Sequence Induction

2. Ventilate to PO2 >13 / PCO2 <5.3 (decreases Cerebral Perfusion Pressure
3. Head up position on bed
4. Osmotic Diuresis (Mannitol/ Hypertonic Saline
5. invasive monitoring - central line/art line/ ICP monitoring
6. Extras - Dex, Antibiotics, Fluids, Vasopressors

Question 58

Hydrocephalus:

i) Definition

ii) Causes

iii) Describe production and circulation of CSF

Answer 58

i) Presence of increased CSF within the ventricular system of the brain

ii) Categorised into:

Communicating (Non- obstructive)

i) reduced absorption - Venous Sinus Thrombosis, haemorrhage

ii) inreased production - Choroid Plexus Carcinoma

Non- Communicating (Obstructive) - Arnold-Chiari Malformation, Colloid Cyst, haemorrhage, abscess, tumour, head injury/oedema

iii) Produced in Ventricular Choroid Plexus:

Lateral ventricles –> Third Ventricle (via foramen of monroe) –> Fourth Ventricle (via aqueduct of sylvius) –> Subarachnoid space (Foramen of Luschka/lateral arpetures either side of pons and Foramen of Magendie/median aperture between medulla/cerebellum)

Absorbed by Arachnoid Villi located in the subarachnoid space

Question 59

Types of hypersensitivity reaction

Answer 59

+ ?Type V - Formulation of stimulatory antibodies

Question 60

i) What are the sequalae of T1HS reaction?

ii) What causes airway compromise?

iii) Size Guedel + NP airway

iv) What can interfere with pulse ox readings?

Answer 60

Antigen - IgE(On Mast Cell) Linking –> Degranulation of mast cell releasing inflammatory cytokines:

Histamine, Leukotrienes, Prostoglandins

–>

Vasodilation, Smooth Muscle Spasm, Vascular Permeability, Increased secretions

–>

Symptoms -> Tingling, Itching, Flushing, Urticaria, Mucosal Oedema, Upper Airway Compromise, Decreased SVR, Hypotension + CV compromise

ii) Airway compromise caused by - Bronchospasm + oedema

iii) Guedel - Incisors –> Angle of Mandible

NP - External Nares –> Tragus

iv) Nail Polish, Peripherally shut down, Carbon Monoxide (overestimate), Bilirubin (Underestimate)

Question 61

i) Constiutents of NS vs hartmann’s?

ii) Complications associated with Colloids?

iii) What is a colloid?

iv) Colloids vs Crystalloids in sick patients?

v) Distribution of crystalloid? Dextrose?

Answer 61

i) Normal Saline:

154 mmol/L Na+

154 mmol/L Cl-

Hartmann’s:

131 mmol/L Na+

5 mmol/L K+

111 mmol/L Cl-

2 mmol/L Ca++

29 mmol/L HCO3- (in the form of lactate)

ii) Interfere with platelets and vWF, Anaphylaxis, VTE

iii) Colloid - contain large insoluble molecules

Crystalloid - contain water-soluble molecules

iv) SAFE Study - Saline vs Albumin (4%) found no survival benefit between the two.

v) Crystalloid distribution is confined to the ECF compartment:

25% - Intravscular

75% - Extravascular

Dextrose - 5% Dextrose quickly becomes water –>

1/3 - Extracellular (1/4 intravascular 3/4 interstitial)

2/3 - Intracellular

As the overall intravascular contribution of dextrose would be minimal it is not useful in resus situations

Question 62

Levels of care

Answer 62

0 - Ward Care

1 - Ward Care with CCOT input

2 - HDU. One Failing System/ Major Surgery

3 - ITU. >1 Failing System / Advanced monitoring.

Question 63

i) Indications for tracheostomy

ii) Types of trachy

iii) Types trachy tubing

iv) Complications of Trachy

v) What constitutes trachy care

Answer 63

i) Congenital Conditions - Laryngeotracheomalacia, Treacher-Collins Syndrome, Laryngeal Stenosis

Acquired Conditions - Head and neck tumours

Emergency Airway - Ludwig’s Angina, Epiglottitis, Largyngeal Oedema, Upper Airway Trauma

Long term ventilation

ii) Elective Surgical Trachy - Horizontal incision midway between cricoid cartialge and sternal notch

Emergency Surgical Trachy - Vertical incision

[Tracheal access via a) vertical incisions between 2nd - 4th rings b) Bjork flap c) window cut]

Percutaneous - Seldinger technique

Mini-Trachy - 4mm tube through cricothyroid lig. under LA

iii) Material - metal vs plastic

Tube- Fenustrated vs unfenestrated

Cuff - Cuffed vs un-cuffed

iv) Early - Bleeding (Thyr. Isthmus+ AJV), Tracheal inj/, oesophageal inj., RLN Injury, Pneumothorax/mediastinum

Tube related - Displacement, Extubation, blockage

Intermediate - Infection (chest, trachea, wound), Trache-inominate/oesophageal fistula, Tracheal ulceration

Late - Tracheal Stenosis

v) Trachy Care - Humidified oxygen, Regular suction and cleaning of inner tube, Emergency trachy kit availability

Question 64

Causes of hyponatraemia

Answer 64

Hypervolaemic - Ur Na+ <20 - CCF, Cirrhosis, Nephrotic Syndrome

Ur NA+ >20 - Renal Failure

Euvolaemia - Ur Na+ >40 - SIADH (Low serum osmolality, Increased urine osmolality, raised urinary sodium), Hypothyroidism, Low glucocorticoids

Ur Na+ <40 - Dietary, Psychogenic Polydypsia

Hypovolaemic - Ur Na+ <20 - Burns/Skin loss, GI loss

Ur Na+ >20 - Adrenocorticol deficiency, Renal Failure, Diuretics, Cerebral Salt Wasting

Pseudohyponatraemia:

Normal serum osmolality - Lipids / Proteins High (myelomatous states)

High serum osmolality - High glucose, Mannitol, alcohols

Drip arm

Question 65

i) Causes of SIADH:

ii) Rx

Answer 65

i) Drugs - Psychiatric, Opiates, NSAIDs AEDs, Cytoxic

Pulmonary - Malignancy, Pneumonia, PE

Cranial - Tumour, Meningitis, Trauma

Many Malignancies.

ii) Rx - Water Restrict.

Demecloycline - DDAVP Receptor Antagonist

Vaptan - V2 Receptor Antagonist

Question 67

Answer 67

J Osborn Waves - Seen in hypothermia (<32 degrees)

Upward deflection between QRS and ST Segment

Question 68

Clostridium Tetani:

i) Describe

ii) When are you fully vaccinatd?

iii) Exotoxin vs endotoxin?

Answer 68

i) Gram Positive Spore Forming Anearobic bacteria that produces toxin (tetanospasmin)

ii) Full Vaccination is conferred - when you have had all five boosters within a ten year period

iii) Exotoxin - Secreted immunogenic protein from poth Gram + and Gram -. Specific Host Response

Endotoxin - LPS from the cell wall present on gram -. Widespread systemis stress resposne

Question 69

WRT MODS:

i) What is it?

ii) Which organs can fail?

Answer 69

i) Multi-Organ Dysfunction Syndrome

ii) Renal Failure, Intestinal Failure, Cardiovascular Compromise, Liver Failure, Bone Marrow Failure, Respiratory Failure

Question 70

i) Adrenergic Receptors - What acts on them?

ii) When would you consider vasopressors/inotropes?

iii) What’s best for fluid refractory hypotension?

iv) Target for patients in septic shock?

v) What is MAP? Calculate it?

vi) What does CVP Monitoring measure?

Answer 70

i) B1 - Cardiac Muscle –> Inotropic and Chronotropic effect. Dobutamine (increases cardiac output)

B2 - Vascular walls –> Vasodilation. Dobutamine (Reduces Afterload)

A1 - Vascular walls/ Heart. –> Vasoconstriction. Noradrenaline –> Increased Blood Pressure (SVR)

Dopamine 1/2 - Diuresis

Dopamine Administration - has effect on a broad range of adrenergic receptors which differ at different doses.

ii) Hypotension unresponsive to fluid

Tachycardia, Distributive Shock (peripheral vasodilation/ low SVR), Low CO

iii) Dopamine + Noradrenaline

iv) MAP >65 mmHg

Other things to monitor (End-Organ perfusion, BP, HR)

v) MAP = (COxSVR) +CVP

MAP calculation = Diastolic BP + 1/3(SBP-DBP)

vi) Cardiac Filling Pressure which is related to End Diastolic Ventricular Pressure. This is used as a surrogate for preload

Preload cannot be actually measured as it is the stretching of cardiac myocytes before contraction

Question 71

i) Distribution of water

ii) How much water in the 70 kg man?

Answer 71

i) 2/3 Intracellular Water

1/3 Extracellular Water (3/4 - Interstitial 1/4 - Intravascular)

ii) 42L in the 70 kg man (60% of body weight)

Question 72

Define:

i) Respiration

ii) Breathing

iii) Respiratory Failure

iv) Minute ventilation

v) Indications for intubation and Ventilation

vi) Confirmation of ET Tube position?

vii) Components of ventilation

Answer 72

i) Transfer of oxygen from air to tissue/ CO2 from tissue to air

ii) The passing of air in and out of the lungs

iii) Inadequate gas exchange (low O2 / high CO2 in arteries)

Type 1 - PaO2 <6.5

Type 2 - PaCO2 > 6 PaO2 <8

iv) Minute Ventilation - RR x Tidal Volume

v) Low GCS State, Upper Airway Injury/Obstruction, ARDS/TRALI, Chest Injury, Neuromuscular Disease,
Prophylaxis - Smoke inhalation, angiodoema

vi) Chest: Symmetrical chest movements/

Ausculation of air in both lungs not in stomach

Gold Standard - Waveform Capnography

imaging - CXR

vii) Ventilation involves:

a) Ventilator (Insp. + exp. circuits)
- Can be spontaneously controlled
- Volume Controlled
- Pressure Controlled
b) Patient
c) Connection between a and b

Question 73

i) Calculation of Minute Ventilation

ii) Complications of mechanical ventilation

iii) When to consider ventilation wean

Answer 73

i) Minute Ventilation = Tidal Volume x RR

Tidal Volume = 5-10ml/kg

RR-= 15

For a 70 kg man

700 x 15 = 10.5 L

ii) Ventilator Associated Lung Injury - Barotrauma (pneumothorax/mediastinum/emphysema)

VAP, Diaphragamtic Atrophy, CV (Decreased preload/ Stroke Volume), Laryngeotracheal damage

iii) Can be weaned when with trials of spontaneous ventilation:

Fio2< 50 %

Low PEEP (<8cm H2O)

Question 74

i) Risk Factors for development of acute AF after surgery

ii) Mx of Acute new onset AF

Answer 74

i) Preoperative: Age, CV Disease, Comborbidities (thyroid/ Lung disease/ diabetes/ alcoholism)

Postoperative: Hypovolaemia, Electrolyte abnormalities, Infection, Hypoxia, Acute Myocardial Event, Pulmonary Embolus

ii) Ascertain an precedent.

If hypovolaemic/septic - Fluid Resuscitation may be enough

If no adverse features - Pharmacological management with digoxin/amiodarone (guided by medical/cardiology teams)

If adverse features - involve arrest/peri-arrest team and emergency DC Cardioversion/ Pharmacological cardioversion may be required

Question 75

i) Open AAA repair complications

Answer 75

i) Graft Related - Haemorrhage, Infection, Spinal Ischaemia/ Renal Failure/ Ischaemic Bowel, Distal embolus, Graft Thrombosis

Operation Related - Acute Renal Failure, Ischaemic bowel (branch occlusion), Abdominal compartment syndrome, Ileus

Question 76

Causes of ischaemia

Answer 76

Arterial Occlusion

Venous Congestion

Hypoxia - Pulmonary/ Anaemia/ Carbon monoxide poisoning

Impaired tissue oxygenation due to impaired oxygen dissociation

Question 77

i) What does clopidogrel do?

ii) What does aspirin do?

iii) When does more care need to be given to stopping antiplatelet agents?

Answer 77

i) Clopidogrel irreversibly inhibits platelet ADP receptor preventing platelet aggregation

- this lasts for 8 days as the average platelet lifespan is eight days

ii) Non specific COX-1 + COX-2 Inhibitor preventing prostaglandin + thrombaxane generation

- Thromboxane is a promotor of platelet aggregation and activation

iii) When the indication is for stent insertion (cardiac/vascular)

Question 78

Methods for reduction of intraoperative blood loss

Answer 78

Meticulous Haemostasis

Cell Savers

Tourniquets

Optomising coagulation

Physiological Hypotension

Question 79

NSAIDs sytemic effects

Answer 79

GI (Reduced prostalgandin production which contribute to the production of protective mucous) - Dyspepsia, Gastritis, Peptic Ulceration

Renal - Interstitial Nephritis, Reduces afferent vasodilation

Cardiovascular - Salt/Water Retention -> Heart Failure

Coagulopathy - Reduce platelet aggregation (due to reduced thromboxane production)

Bronchospasm- Due to increased leukotriene production

Question 80

i) Metabolic Respone to Injury

ii) What is the respiratory Quotient?

Answer 80

i) Ebb Phase - Reduced metabolic rate/ cardiac output/ core temperature

Flow Phase - Catabolic Phase

then

Anabolic Phase

ii) Respiratory Quotient = CO2 Excreted / O2 Consumed

Used to suss out which foods are being metabolised

Question 81

Why is NJ preferred in pancreatitis to NG?

Answer 81

NJ preferred- as it bypassed the DJ flexure. Fatty Acids in the duodenum cause the release of CCK –> Stimulates pancreatic enzyme secretion and worsen the inflammatory process

Question 82

i) Features of opiate overdose

ii) Managing overdose

Answer 82

i) Confusion, Itchiness, Visual/Tactile Hallucinations

Hypotension, Pinpoint Pupils

Apnoea, Respiratory Failure

ii) A-E approach

Nalaxone following trust policy (0.4-2mg IV which can be repeated evert few minutes up to 10mg)

Contact critical care team regarding Nalaxone infusion

Question 83

Causes of pancreatitis

Answer 83

Idiopathic

Gallstones

Ethanol

Trauma

Steroid

• *M**umps
• *A**utoimmune

Scorpion bite

Hypercalcaemia/hyperlipidaemia

ERCP

Drugs (Azathiaproine, Sulfasalazine, Trimethoprin, Tetracycline)

Question 84

Define: Shock

Answer 84

Inadequate tissue perfusion for metabolic requirement

Question 85

Classification of Shock

Answer 85

Question 86

TURP Syndrome

i) Features

ii) Rx

Answer 86

i) Hyponatraemia - restlessness, blurred vision, confusion

Hypovolaemia - overload/cardiac failure

High Ammonia - Confusion

This is due to the glycine rich instillation fluid used which when asborbed causes a:

dilutional hyponatraemia

raised ammonia

ii) If intraoperative - stop and stop instillation of fluid

C- A-E Assessment:

Consider intubation if necessary

Take bloods and an ABG to look at the electrolytes

Enlist anaesthetist/ITU support in maanaging the electrolytes as the patient is also overloaded

• ?hypertonic saline
• ?fluid restrict
• ?diuresis

Treat complications such as arrhythmias/ seizures

Question 87

Diuretics MOA

i) Loop

ii) Thiazide

iii) Aldosterone Antagonist

iv) Amiloride

v) Osmotic Diuretic

Answer 87

i) Loop - Furosemide, Bumetanide

Inhibit Na/K/Cl- Transporter in the thick asending loop of henle. Prevents sodium resorption/concentration gradient formation. Prevents concentration of urine.

ii) Thiazine - Bendroflumethiazide

Inhibits Na/Cl- transporter in DCT.

iii) AR Antag. - Spironolactone, eplenorone

Prevents the insertion of eNAC channels in the collecting tubules which prevents Na+ resorption and K+ excretion

iv)Amiloride - K+ Sparing diuretic

v) Osmotic Diuretic - Mannitol. Large molecule that is filtered but not reabsorbed. Causes water to be retained in the tubules.

Question 88

Classic time for anastamotic leak

Answer 88

Day 4/5

Question 89

Causes of post-operative pyrexia

Answer 89

Blood - Transfusion

Physiological - SIRS (0-1 Days)

Infection - Pulmonary atelectasis (1-2) days, UTI, Cellulitis, SUperficial thrombophelbitis, Wound Infection

Drug Reaction - Suxamethonium

Anastamotic leak (4-5 days)

Thrombosis - PE, Pneumonia

Question 90

i) Risk of aortic stenosis in surgery?

ii) Coronary Perfusion Pressure Equation

iii) Voltage criteria for LVH

iv) Warfarin MOA

Answer 90

i) Due to the outflow obstruction there isn’t a capacity to modulate cardiac output!

Anaesthetic agents/ spinal anaesthetics can reduce the afterload/SBP.

Myocardium is compromised due to lack of coronary perfusion

ii) Coronary Perfusion Pressure = Systemic Diastolic Pressure - LV End Diastolic Pressure

iii) Either S in V1 or R in V5/V6 >35 mm / 7 small squares

iv )Warfarin - Inhibits Vitamin K Epoxide Reductase

Question 91

i) What are the desired effects of sedatives?

ii) Contraindications to sedation?

iii) General risks to sedation?

iv) Monitoring requirement for sedation?

Answer 91

i) Reduced state of consciousness, analgaesia, anxiolytic

Light - Patient can maintain their airway and respond to stimuli easily

Deep - Patient airway is not always patent and needs sizable stimuli to rouse

GA - Patient airway is not patent and they are not responsive

ii) CIs to sedation - patient choice, long procedures, lack of monitoring, not starved appropriately (food >6 hours, water >2 hours), unstable patients.

iii) Risks - Respiratory Depression, Airway Compromise, Confusion, Hypotension, Impaired gastric emptying/ regurgitation

iv) Monitoring - General Obs, Three lead ECG, ETCO2, If conscious then monitoring of symptoms

Question 92

Features of different sedation agents:

i) Midazolam

ii) Ketamine

iii) Propofol

iv) Nitrous Oxide

v) Morphine

vi) Etomidate

Answer 92

i) Midazolam. 1-2mg. Good for amnesia/anxiolytic. not for pain. Minimal cardiorespiratory compromise

ii) Ketamine. Good for amnesia/Pain. Marked dissocative psychiatric effects / nausea/ vomiting.

iii) Propofol. Rapid Onset. CVS/Resp Depression. Good antiemetic properties

iv) Nitrous Oxide. Inhaled. SACD in chronic use.

v) Morphine. Good for pain. Caution in renal patients. Causes vomiting/constipation/ nausea/ CV+ resp compromise.

vi) Etomidate. Induction agent. Adrenocortical suppression. Less CV/Resp effect.

Question 93

Signs of Lidocaine Toxicity

Max dose w/ w/o adrenaline

Answer 93

Max Dose: With adrenaline - 7 mg/kg . Without adrenaline 3mg/kg

Signs of toxicity:

Perioral Paraesthesia

Hypotension

Convulsions

Dizziness

Cardiac Arrhythmias

Collapse

Question 94

Nutritional Requirements:

Sodium

Potassium

Calories

Protein/Fat/Glucose

Answer 94

Sodium - 1-2 mmol/kg/day

Potassium - 1mmol/kg/day

Calories - 25-30 kcal/kg/day

Protein/Fat/Glucose - 20:30:50

Question 95

Adrenaline vs Noradrenaline

Answer 95

Adrenaline Alpha and Beta Noradrenaline predominantly alpha Alpha - peripheral vasoconstriction Beta - cardiac chronotropic and inotropic

Question 96

What is dopexamine

Answer 96

Splanchnic vasodilator

Question 97

Anion Gap

Calc

Causes

Answer 97

Calculation (Na+K+)-(Cl+HCO3)

Normal 10-18

Low Anion Gap

hypoalbuminaemia, increased cations (MG++, Ca++, IgG),

Normal Anion Gap - Hyperchloraemic

Bicarb Loss, Renal Tubular Acidosis (moreso in type II), Drugs (Acetozolamide), Chloride Injection, Addison’s Disease (Type IV RTA)

High Anion Gap

Lactate, Ketoacidosis, Urate, Exogenous Acids

Question 98

JVP

Absent a waves

Large a waves

cannon waves

prominent v waves

slow y descent

steep y descent

JVP rises during inspiration

Fixed Raised JVP

Answer 98

Absent A Waves - AF

Large A Waves - Right ventricular hypertrophy, triscupid stenosis

Cannon Waves - Complete Heart Block

Prominent v waves - Tricuspid Regurgitation

Slow y descent - Tricuspid stenosis, Right Atrial Myxoma

Steep y descent - Right ventricular failure, Constrictive pericarditis, Tricuspid regurgitation

JVP rises during inspiration - Kussmaul’s sign of constrictive pericarditis

Fixed Raised JVP - Superior Vena Cava Obstruction

Question 99

Four mechanisms of vomiting

Answer 99

Gag - Touch Receptors in throat (CN IX), Pharyngeal Cosntrictors (CNX + CNIX for stylopharyngeus)

Labyrnthine disorders - Motion Sickness

Stomach and duodenal distension - stretch receptors

Central (brain) - chemically induced (drugs etc.)

Question 100

When to admit for acute lower GI bleeding

Answer 100

Age >60

Significant Co-Morbidity

Unstable

Profuse bleeding

Aspirin/NSAID use

Question 101

By what mechanism does ECF Volume depletion cause Metabolic Alkalosis

Answer 101

Losing significant bodily fluid through vomiting or diuretics results in a loss of Na+ + Cl-

This leads to RAAS activation –> aldosterone causes increased ENaC channels so more Sodium crosses from lumen into cells.

Luminal K+ channels upregulated so potassium is lost to the lumen.

Na+K+ATPase at interstitial side of cells is upregulated —> K+ is moved into the cell whereas Na+ is moved into interstitium.

These three transporter changes lead to an increase loss of K+ to the collecting duct lumen and a preservation of Na+

Loss of K+ Leads to K+/H+ Buffering. K+ moves from cells into ECF in exchange for H+ —–:> Alkalosis

Question 102

Managing local anaesthetic toxicity

Max Doses

Answer 102

Intralipid:
Bolus- 1.5 ml/kg over 1 minute

Infusion - 0.25 ml/kg/minute

If prilocaine is used then administere methylene blue

1st dose - neat/ 2nd dose w/adrenaline

Lignocaine - 3 mg/kg. 7 mg/kg

Bupivicaine - 2 mg/kg 2 mg/kg

Prilocaine - 6 mg/kg 9 mg/kg

Prilocaine

Question 103

Best test for vWD

Answer 103

Bleeding Time (factor VIII may also be low)

vWD can be Autosomal Dominant:

Type I - Quantitative deficiency of vWF

Type 2 - Qualitative impariment of synthesis of vWF

Autosomal Recessive

Type 3 - Absolute deficiency in vWF

Question 104

Which Coag factors to the following influence:

Heparin

Warfarin

Liver Disease

Disseminated Intravascular Coagulation

Answer 104

Heparin - 2,9, 10, 11

Warfin - 2, 7, 9 , 10

Liver disease - 1, 2 , 5 , 7, ,9, 10, 11

DIC - 1, 2, 5, 8, 11

Question 105

Which hormones are reduced in stress response?

Answer 105

Insulin

Oestrogen

Testosterone

Question 106

principles for operating in acute cholecystitis

Answer 106

<48 hours surgery is a good idea

>5 days - surgery is best left deferred to 3 months to allow inflammation to settle

Question 107

Fistulae

When is it safe to conersvatively manage?

Drug therapy for high output fistula

Contraindication to probing perianal fistulae

How to delinieate fistula tract?

Answer 107

Conservative management - In the absence of IBD or distal obstruction

Octreotide si used to reduce pancreatic secretions in the context of high output fistulae

Perianal fistulae should not be probed in teh context of acute inlammation

Fistula anatomy can be delineated using CT and barium studies

Question 108

Why use bupivicaine post-operatively over lidocaine?

Answer 108

It has a much longer duration of action than lignocaine and therefore can provide longlasting wound-site analgaesia

Question 109

What would be the LA of choice in regional block?

Answer 109

Prilocaine - this is much less cardiotoxic

Question 110

Sulphur Granules and Gram Positive Organisms - Histology

Answer 110

Actinomycosis

• Forms multiple sinuses

The sulphur granules (round or oval basophilic masses)

Question 111

Within what time should an open fracture be internally fixated?

Answer 111

72 hours

Question 112

Scaphoid abdomen

Answer 112

Abdomen sucked inwards:

Think diaphragmatic hernia in newborn

Question 113

Wound healing - Predominant Cell Types

Inflammation

Regeneration

Remodelling (Contraction)

Answer 113

Inflammation

Neutrophils. Early phase (first week)

Regeneration

Fibroblasts. (8 weeks)

Microvascularisation

Remodelling (Contraction)

Differentiated fibroblasts.

Microvessels regress so the scar looks pale.

Question 114

Ileostomy effluent

Answer 114

Na - 126 mmol/ L

K+ - 22 mmol/L

Question 115

What is in cryoprecipitate

Answer 115

VIII

Fibrinogen

XIII

vWF

Question 116

Ventilation

What are the three cerebral areas responsible for ventilation and what do they respond to?

Any non-cerebral areas involved?

Answer 116

Medulla Oblongata

This responds to increased interstitial H+ to increase ventilation (to blow off CO2). The Apneustic Centre in pons instigates inspiration whereas the Pneumotaxic Centre, also in the pons, inhibits inspiration.

Peripheral chemoreceptors are in the carotids and arch of aorta –> these respond to arterial pO2, pCO2 and H+

Question 117

Below which blood pressure does renal autoregulation of flow fail?

Answer 117

<80 systolic blood pressure

Question 118

Management of traumatic pneumothorax and why?

Answer 118

Chest drain - Usually in context of traumatic pneumothorax there is damage to lung parenchyma = High chance of tension pneumo development

Question 119

Which drug prevents conversion of plasminogen to plasmin?

Answer 119

Tranexamic Acid

Question 120

Which clotting factors are particularly heat sensitive?

Answer 120

Factor V

Factor VIII

Hence FFP is frozen

Question 121

Dose of heparin for:

Vascular Bypasses

Cardiopulmonary bypasses

Answer 121

Vascular Bypasses

3000 units prior to cross clamping

Cardiopulmonary bypasses

30,000 units priot to initiating bypass

Question 122

Actions of PTH

Answer 122

Bone - Osteoblasts binding –> inreased RANKL expression –> Activation of osteoclasts —> increase resorption

Kidney - Resorption of calcium and mangesium from DCT. Decreased resorption of phosphate

GI - PTH increases Vit D activation –> increased GI calcium absorption

Question 123

in DIC which components of clotting are depleted fastest

Answer 123

V, VIII and Platelets

Question 124

Effects of Adrenaline

Answer 124

Alpha -

Peripheral Vasoconstriction

Insulin inhibition

Glycogenolysis in liver/muscle and glycolysis in muscle

Beta -

1 - Cardiac chronotrope + inotrope, increased renin secretion

2 - Skeletal muscle vasodilation + coronary artery vasodilation. Bronchodilation

Glucagon secretion, ACTH secretion, Lipolysis in adipose tissue

Question 125

DTPA vs MAG3

Answer 125

DTPA - good for assessment of GFR

MAG3 - good for assessment of renal function in patients with known impairment

Question 126

Rockall Score

WHen?

Components?

Answer 126

Following Endoscopy for UGI haemorrhage

Components:

A Age

B BP

C Co-morbidities

D Diagnosis

E vidence of bleeding

Question 127

Kocher Criteria for Septic Arthritis

Answer 127

WIFE

WCC >12

I - inability to weight bear

Fever

ESR >40

Question 128

Drug Treatment for Colonic Pseudoobstruction

Answer 128

Neostigmine

Question 129

management for biliary leak post lap chole

Answer 129

ERCP + Stent

Question 130

Biliary Decompression as an adjunct to curative pancreatic surgery

Answer 130

ERCP + Stent

Do not surgically bypass them

Question 131

Management of sudden full dehiscence

Answer 131

Analgaesia,

IV fluid,

IV abx

Cover wound with saline gauze

Return to theatre STAT

Question 132

BEst way to assess for upper airway compression?

Answer 132

Flow Volume Loop

Question 133

Anaerobic Organism complicating difficult operations>

Answer 133

Bacteroides Fragilis - Gram Neg, Anaerobe, Rod Shaped

Involved in majority of peritoneal infections

Question 134

What does serotonin do to vessels?

Answer 134

Intact vessels - Vasodilation

Damaged vessels/tissue - vasoconstriction

Question 135

Four drugs commonly associated with parotid enlargement

Answer 135

Thiouracil

Isoprenaline

Phenylbutazone

Oestrogen Contraceptic pills

Question 136

Drug cause of SIADH

Answer 136

Carbamezapine, SSRIs, Sulfonylureas, TCAs, vincristine, cyclophosphamide

Question 137

ABx MOA

Inhibiting Cell Wall FOrmation

Inhibiting Protein Synthesis

Inhibiting DNA Synthesis

Inhibiting RNA Synthesis
Cell Membrane

Answer 137

Inhibiting Cell Wall FOrmation

Penicillin, Cephalosporin, Glycopeptide

Inhibiting Protein Synthesis

50S - Macrolide, Linezolid, Chloramphenicol

30 S - Aminoglycloside, Tetracycline,

Inhibiting DNA Synthesis

DNA Gyrase - Fluroquunilone

Metronidazole, Sulphonamide, Trimethoprim

Inhibiting RNA Synthesis

Rifampicin

cell Membrane

Polymxin

Question 138

Perforated appendicitis - where is fluid most likely to collect

Answer 138

pelvis

Question 139

Mediators of acute inflammation

Answer 139

Serotonin

Histamine

Prostaglandin

Leukotrienes

TNF

Interleukins

Question 140

Why might the APTT be long in someone with Anti Phospholipid Syndrome?

Answer 140

They might have Lupus Anticoagulant.

ALthugh in vivo this is prothrombotic, in vitro it increases APTT

Question 141

Actions of corticosteroids

Answer 141

Metabolic

Decreased uptake/utilisation of glucose

Increased gluconeogenesis

Increased hyperglycaemia

Increased protein catabolism

Lipolysis

Regulatory

Negative feedback on hypothalamus

CNS - decreased vasodilation/ decreased fluid exudation

Decreased osteoblastic/ Increased osteoclastic

Decreased inflammation

Question 142

Treatment of pancreatitic pseudocyst

Answer 142

Endoscopic or radiological cystgastrostomy

Question 143

Laparotomy approach in children

Answer 143

Transverse Supra Umbilical incision

Question 144

Trotter’s Triad

Answer 144

Nasopharyngeal Carcinoma

Unilateral Conductive Hearing Loss

Ipsilateral Facial Pain

Ipsilateral Palatal Paralysis

Question 145

How does tranexamic acid work>

Answer 145

Inhibits plasmin which is responsible for fibrin degradation

Question 146

Where is the intercostal bundle

Answer 146

Lies in the subcostal groove

Vein is most superior (least easily damaged)

Artery

Nerve (most inferior)

Question 147

Which surgical device is good for managing splenic bleeding?

Answer 147

Argon plasma coagulation system

Question 148

Which clotting constituents are consumed most quickly in DIC

Answer 148

V, VIII and platelets

Question 149

Treatments for extravasation injury

Doxirubicin

Contrast media, TPN, Vinca Alkaloids

Vinca Alkaloids ALone

Answer 149

Doxirubicin - COld Compress

Contrast media, TPN, Vinca Alkaloids - Hyaluridonase

Vinca Alkaloids ALone - Warm Compress

Question 150

Potential Blood Loss from:

i) Humeral #

ii) Tibia #

iii) Femur #

iv) Pelvic #

Answer 150

i) Humeral # - 750ml

ii) Tibia # - 750ml

iii) Femur # - 1L

iv) Pelvic # - 3L

Question 151

Steroids:

i) What is a steroid?
ii) Anatomical layers of adrenals and steroids they produce
iii) What causes increase in aldosterone production? What acid/base abnormality can increased aldosterone cause?
iv) What causes GC production?

Answer 151

i) Hormonal compound formed from 4 cycloalkane rings

ii) Glomerulosa - Mineralocorticoids

Fasciulata - Glucorticoids

Reticularis - Sex Hormones

Medulla - Catecholamines

iii) Aldosterone production is caused by:

a) Incr. Renin b) Hyperkalaemia c) Hyponataraemia

It can cause a metabolic alkalosis due to K+ excretion (consequnetly H+ being transported intracellularly in exchange for K+)

iv) The HPA Axis - Hypothalamus - CRH/ Pituitary - ACTH / Adrenal - Glucocorticoid

Question 152

i) Main effects of glucocorticoids

ii) Hormones produced by the Anterior Pituitary?

Answer 152

i) Hyperglycaemia - Increased gluconeogenesis / Antagonising Insulin

Protein - Stimulates hepatic protein synthesis/ Reduced peripheral protein synthesis

Fat - Stimulates lipolysis

Kidneys - Exerts mineralocorticoid effect in increased concentrations

Stress - Key modulator in the body stress response

Anti- Inflammatory + Immunosuppressive

Other - Weight Gain, Osteoporosis, Capillary Fragility, Proximal Myopathy, Peptic Ulcer, Psychiatric

ii) Anterior Pituitary:

ACTH, TSH, LH, FSH, Prolactin, Growth Hormone

Question 153

Addisonian Crisis:

i) 4 Major Features

ii) What is a crisis?

iii) Mx of a crisis

iv) Who doesn’t need perioperative glucocorticoid coverage?

v) When to cover for glucocorticoid insufficiency perioperatively?

vi) How to test adrenal function ?

vii) how to cover with steroids perioperatively?

Answer 153

i) Major: Shock

Abdominal Pain

Nausea Vomiting

Temperature dysregulation

Other: Hyperkalaemia, Hyponatraemia, Metabolic Acidosis

ii) Addisonian crisis is where the glucorticoid supply is insufficient to meet the glucorticoid demand:

Primary - Adrenal Insufficiency

Secondary - Exogenous Steroids abruptly stopped/not increased

iii) ATLS/ CCrisp approach

IV Hydrocortisone 100mg QDS

IV Fluids

Electrolyte management

iv) No need for steroid change if:

a)Steroid administration <3 weeks

b) 5mg prednisolone OD (or equivalent)/ 10mg prednisolone Alternate Days (or equivalent)

v) Perioperative coverage should be for patients:

a) Cushing’s Syndrome on exogenous steroids

b) Known to be addisonian and receiving steroid treatment

c) On >20 mg prednisolone OD (or equivalent)

d) Stopped high dose steroids in the last 3 months

vi) Adrenal Testing through early morning cortisol and ACTH stimulation test

vii) Minor Procedures - usual morning dose and 25mg at induction

Moderate Procedures - usual morning dose and 25-50mg hydrocortisone at induction and 25 mg hydrocortisone every 8 hours for 24 hours

Major procedures - usual morning dose and 50-100mg hydrocortisone at induction and 50 mg every 8 hours for 24 hours and then reduce by half a day until reaching maintenance

Question 154

ASA Grading

Answer 154

I - No Comorbidities

II - Mild Systemic Disease

III- Severe Systemic Disease

IV - Severe Systemic Disease that is a constant threat to life

V - Moribund person who will die without operation

VI - Brain Dead who is having organ removal for donor purpose

Question 155

LEMON classification system for difficult intubation

Answer 155

Look for visible risk factors - facial trauma/ small mandible/ short neck

Evaluate - 3 - 3 -2 rule.

3 fingers - between incisors

3 fingers - between hyoid bone and chin

2 fingers - between thyroid notch and floor of mouth

Mallampati Score - tongue to mouth opening size (ease of laryngoscopy)

Obstruction - Trauma/Swelling

Neck Mobility - C Spine injury/ Rheumatoid Arthritis

Question 156

Coroner Referrals

Answer 156

1. Death <24 hours after admission
2. Suspicious/ accidental/ violent/ suicide deaths
3. Death after operation/procedure
4. Unknown cause of death

Question 157

What types of response are there to a fluid challenge?

Answer 157

i) Full Responders - Probably only mildly hypovolaemic

ii) Transient Responders - Likely to be hypovolaemics so need more fluid resusictation with fluids

• This can also represent a person who is actively haemorrhaging so this needs to be considered

iii) Non responders - These patients are either profoundly hypovolaemic or there is another cause than hypovolaemia contributing to their hypotension

Question 158

i)How to approach a trachy patient in respiratory distress?

ii) What are the components of a trachy kit?

Answer 158

i) Some help would be handy

a) Ensure patient is monitored

b) Look for chest wall movement ( reassures you that they are having air entry )

c) Listen for breath sounds in the tracheostomy tubing itself

d) Feel for air coming from the tracheostomy

e) Find out if the trachy has an inner tube/if it is cuffed

f) Try to suction the tube –> If this fails then go to g) and h)

g) With inner tube- Take the inner tube out and clean it/ change it

h) Without inner tube - Towel underneath shoulders and change the tube keeping the stoma open with forceps

ii) Trachy Kit

2 x Trachy Tube (one same size + one smaller)

Bag and Mask

Portable Suction Device + catheter

NaCl Ampoule + syringe

Question 159

Indications for Renal Replacement Therapy

Answer 159

Anuria/Oliguria (persistent)

Refractory Hyperkalaemia

Ureamia (+complications)

Pulmonary Oedema

Drug Overdose

Severe Acidosis

Question 160

Types of transplant rejection

Answer 160

Question 161

Types of Immunosuppresant

Answer 161

Corticosteroids

Calcineurin inhibitors - Tacrolimus, Cyclosporin

Anti-purine - Azathioprine, Mycophenolate

Cytotoxics - Cyclophosphamide

Antimetabolite - Methotrexate

Small molecule inhibitors - -ibs

Antibodies - abs

Question 162

What are the constituents of :

i) FFP

ii) Cryoprecipitate

iii) Prothrombin Complex Concentrate

Answer 162

i) FFP - Albumin, All clotting factors, vWF, Complement, Fibrinogen

ii) Cryoprecipitate- VIII, XIII, vWF, Fibrinogen

iii) Prothrombin Complex Concentrate - II, (VII), IX, X, C, S, Heparin

Question 163

Vomiting:

i) Classcial Biochemical Abnormality?

ii) ECG Changes in hypokalaemia?

Answer 163

i) Hypokalaemic, Hypochloraemia Metabolic Alkalosis

Due to:

a) loss of HCl + K+ from gastric secretions

b) Hypovolaemic/Hyponatraemic mediated RAAS Activation leading to K+ excretion in the collecting tubules

ii) Flat/Inverted T Waves, U Waves, Long PR, ST depression

Question 164

Describe

Management

What delays wound healing/fracture healing

Answer 164

Weber C Ankle Fracture ( Weber classification by the distal fibular fragment. A - Below syndesmosis. B - through sydnesmosis. C - above syndesmosis)

Management - would consult BOAST Guidelines

SHould not have had X ray as tehre would have been obvious deformity. Needs urgent reduction.

• Make sure neurovascularly intact
• Reduction by lifting toes with hand under calcaneum and longitudinal traction.
• Check x ray and re-cehck neurovascularly intact after reduction
• Below knee plastering
• Will need ORIF (either within 24 hours or after 6 days - this is due to swelling)

Complicated by :

Co Morbidities - Age, Vascular Disease, Diabetes, neuropathies

Smoking

MEdications - NSAIDs, Steroids

Question 165

What does intact bulbocavernosus reflex intact in the context of acute paralysis?

Answer 165

This reflex involves pulling clitoris/ or glans penis and assessing reflex anal sphincter contraction. (S2- S4). Can also be tested by tgging a catheter

Intact - Spinal Severance

Not Intact- Spinal Shock

Question 166

Assessment in ?spinal injury

Define cauda equina syndrome

Red Flag syptoms for back pain

Answer 166

History -

Pain- Characteristics (neuropathic, ?bilateral)

Urinary function - ?feel full bladder, ?pass urine, ?control stream ?does she void normally at all

Bowel Fucntion

Examination

LL / UL exam

Reflexes

Perianal paraesthesia - sharp testing

Anal tone testing

Bulbocavernosus reflex testing

Cauda Equina Syndrome:

• Back pain, Neuropathic pain, lower limb weakness, perianal paraesthesia, visceral dysfunction

Red Flag Symptoms

TUNA FISH

Trauma, Unexplained weight loss, Neurological Symptoms, Age >50

Fever, IVDU, Steroid Use, History of cancer

Question 167

All Dermatomes and Myotomes

Answer 167

Question 168

i) Management of intertrochanteric NOF

ii) Classification systems from extracapsular NOF

Answer 168

i) Reduction - In traction stirrup (protected with wool)

• Longitudinal traction with patella facing the ceiling and then check x ray before fixing

ii) Intertrochanteric Fracture - Evan’s Classification (1-5). 1 is undisplaced and 5 is displaced + severely communited

Subtrochanteric Fracture - Russel Taylor Classification System

Question 169

i) Intracapsular NOF Management

ii) Intracapsular NOF Classification

Answer 169

i) Non displaced - Can try cannulated screw/DHS

Displaced and patient is independently mobile, cognitively intact + fit for surgery - THR otherwise hemiarthroplasty

ii) Intracapsular NOF:

Pauwel’s - Angle of fracture

Garden’s - based on valgus dispalcement

Question 170

i) What is acute tubular necrosis + causes

Answer 170

i) Renal failure due to insult to tubular epithelial cells due to either:

Ischaemia

Nephrotoxins - Myoglobin, Antibiotics (Aminoglycosides), Toxins (heavy metals)

Question 171

Some complications of cholecystitis

Answer 171

Chronic Cholecystitis

Gallbladder mucoceoele

Gallbladder empyema

Gallstone Ileus

Gallbladder perforation

Question 172

Risks on consent form for laparoscopy +/- appendicectomy

Answer 172

Bleeding, Infection, Damage to structures, Pain post-procedure, Anaesthetic Risk, Requirement to open abdomen to resect more bowel / form a stoma

Question 173

Management of anterior shoulder dislocation

Answer 173

Analgaesia

Neurovascular status

X Ray

Reduction with analgaesia:

Hippocratic - axilla countertraction

Stimson - prone with arm hanging over bed and gentle traction for 15-20 minutes

Post reduction chest x ray and neurovascular check

Polysling for 4 weeks after to allow soft tissue healing

Question 174

Supracondylar fractures

i) Common nerve palsies

ii) How would you assess nerve function of someone in backslab?

iii) What would you consent the patient for if closed reduction and percutaneous pinning being planned?

iv) Classification for supracondylar fractures?

Answer 174

i) Extension - Median nerve AIN branch > Radial Nerve

Flexion - Ulnar nerve

ii) Median Nerve - Test FDP and FPL (Ok Sign)

• Index finger sensation

Ulnar Nerve - Intrinsic hand muscles abduction and adduction of middle / index fingers

• Little finger sensation

Radial Nerve- Extension of MCPJ

• 1st Dorsal web space

iii) Scar, Infection of metalwork, Vascular Injury, Nerve injury, Conversion to open procedure, COmpartment syndrome, Deformity, Mal-union, Non-union

iv) Gartland I - Non displaced

II - Angulated with intact posterior cortex

III - completely displaced

Question 175

Haematemesis

i) Causes

ii) Is initial Hb reading accurate?

iii) Management

Answer 175

i) Oesophageal - Ulcer, Varices, Mallory Weiss Tear, Malignancy, Fistula

Stomach - Ulcer, malignancy, angiodysplasia, varices,

Duodenum - ulcer, malignancy, angiodysplasia, varices

ii) No it can be falsely raised as it takes time for the interstitial fluid to redistribute its volume to the plasma.

iii) A-E approach cCRISP

Replace circulatory volume

Stop anticoagulants

Give blood ( activate massive transfusion protocol i needed)

IV PPI

Antibiotics/ Terlipressin if suspect varices

Urgent endoscopy

Question 176

Risk factors for anastamotic leak

Answer 176

Patient - SMoking, vascular disease, diabetes, steroid use, nutrition

Pathology - IBD, Autoimmune, Collagen disordes

Technical - site of anasatmosis, quality of anastamosis, blood supply to the two ends, infection

Question 177

i) Mx of severe Crohn’s Flare

ii) Cx fo crohn’s disease

Answer 177

i) Truelovv and Witt’s Criteria

Admit.

IV Steroids, Fluids, antibiotics ( metro/ cipro ),

Infliximab if not improving

ii) Cx:

Abscess, fistula, SBO, toxic megacolon, malignancy, PSC,

Surgery related - Gallstones, Short bowel syndrome, malabsorption, further fistulae

Extra intestinal manifestations- eye disease, joint disease

Question 178

Differences between Crohn’s and UC

Answer 178

Question 179

Arrhythmias

i) Causes of AF

ii) When to anticoagulate in AF

iii) Tachycardias

iv) Bradycardias

Answer 179

i) P - neumonia, COPD, PE

I- diopathic, ischaemic heart disease R- heumatoid arthritis, respiratory disease A-trial enlargement T-hyroid disease, caffeine, other stimulants E- ethanol S- epsis/ sleep apnoea

Volume depletion

ii) CHADS VASC - CCF, Hypertension, AGE >70, Diabetes, Stroke

iii) AFlut, VT, SVTs

iv) Heart block, Sinus arrhythmia, Sinus Bradycardia, Drugs, Hyperkalaemia

Question 180

i) You see Acute STEMI on ECG

ii) Complications of acute MI

iii) Investigations

Answer 180

i) Assess the patient.

MONA BASH

Morphine, Oxygen (if hypoxic), Nitrates, Aspirin

Beta blocker (within 12 hours, ACE - i (within 24 hours), Statin, Heparin (For NSTEMI)

Discuss with interventional cardiologist - ?reperfusion ?thrombolysis

ii) Complications -

Acute - Rhythm disorders (Heart block, AF), Conduction disorders (BBB)

Heart Failure

Papillary muscle rupture/infarction

Rupture of IV Septum

Mural THrombus

THromboembolism

Pericarditis

Chronic - Dressler’s Syndrome (pericarditis), Rhythm disorder, rate disorder, heart failure

iii) immediately - Serial troponin (I or T) (0 hour -12 hour)

Question 181

Causes of post operative confusion

Answer 181

Infective - Wound, chest, urine, abdominal

Metabolic - Oxygen, Hb, Sodium, Calcium, sugar, hepatic, renal

Drug causes - Benzos, alcohol withdrawal, anticholinergics, anticonvulsants, steroids, opioids

Vascular causes - Stroke, intracerebral bleed

Question 182

Six life threatening injuries that might be found during primary survery

Answer 182

ATOMFC

Airway Obstruction,

Tension Pneumo

Open pneumothorax

Massive haemothorax

Flail Chest

Cardiac Tamponade (low BP, engorged neck veins, muffled heart sounds)

Question 183

Immediate CT Head for..

Answer 183

GCS <12

GCS <15 after 1 hour

Suspicions of base of skull/depressed skull

2 or more vomiting

Retrograde amnesia

persistent headache

Focal neurology

Age Elderly and Young

Bleeding diathesis

Question 184

i) Young intracapsular NOF management

ii) Nerve at risk during posterior approach, lateral approach

Answer 184

i) Goal is to restore function and preserve the hip unlike with an elderly NOF where you just want them on their feet again.

Need to achieve satisfactory reduction and ideally cannulated screw/DHS

Long term management will involve NWB for 6 weeks (unlike elderly who you weight bear immediately to avoid secondary complications such as VTE/infection)

ii) Posterior - sciatic

Lateral- Sup. Gluteal nerve

Question 185

Open fracture management

Answer 185

NV Status/ wary of compartment syndrome

IV antibiotics

Reduction and splinting

Saline gauze

Debridement +/- Soft tissue coverage

Soft tissue coverage/ amputation within 72 hours

Question 186

i) Pelvic fracture mx

ii) X ray views for acetabular fractures

Answer 186

i) In line with BOAST guidelines

ATLS approach

Pelvic Binder - Across GTs.

If unstable - Fast Scan, Angiography, Pre-peritoneal packing, laparotamy

If stable - CT Scan

Urological injury (Difficult catheterisation, blood at the meatus) - CT Urethrography/cystography. Urology input

Open injury - ?Colostomy ?bladder drainage

ii) Judet views- 45 degree obturator and iliac oblique views

Question 187

Important progonstic indicators in trauma patietns

Answer 187

Lethal Triad - Acidosis, Hypothermia, Coagulopathy