Critical Care Qs Flashcards
Post - Op Colectomy
Tachycardic and Unwell
i) Differentials
ii) Investigation of choice for PE
i) Differentials
Anastamotic leak, VTE, ARDS, Infection
Late- Wound Infection, Post-operative collection,
ii) CTPA - look for filling defect in the pulmonary arteries
Trauma Patient - LOC + Vomiting + Concomitant ankle fracture
GCS subsequently Drops
i) Points of contact
ii) Possible CT Head findings
iii) Early CT Head Criteria
i) Contact - Anaesthetist/ITU, Neurosurgeons, Radiology, Senior Support
ii) CT Head findings - EDH, SDH, Contusion, DAI
iii) Canadian CT Head Rules - CT required for minor head injury if :
GCS < 15 After 2 Hours
>2 Episodes Vomiting
Depressed Skull Fracture Concern
Base of SKull Fracture Concerns
Age >65
Medium Risk - Retrorade amnesia, Dangerous Mechanism
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?
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 CO2 leads to vasoconstriction
High CO2 leads to vasodilation
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
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
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
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
Criteria for malnutrition
i) Bmi <18.5
2) Weight loss of 2.3kg/ 5% in 1 month
3) Weight loss of 4.5kg/10% in 6 months
Contraindications to enteral feeding?
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
Contraindicatiosn to parenteral nutrition?
i) Hyperosmolarity
ii) Severe hyperglycaemia
iii) Volume overload
iv) Poor IV access
Feeding Calculations
i) in normal weight/ underweight
iii) obese patients
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
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
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
i) Complications Enteral
ii) Complications Parenteral
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
ARDS
1) Causes
2) Features
3) Pathology
4) Management
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)
i) Constituents
ii) Pulse deficit?
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.
1) Intitial Stabilisation
2) Type 2 RF
3) Initial Management
4) Initial Imaging
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
1) Types of shock
2) BP components
3) Shock Categories
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
What to say in the case of a septic patient?
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%
i) Bloods for patient with abdominal pain + SIRS
ii) Imaging for same clinical scenario
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)
Scoring Systems for Pancreatitis:
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
i) Potential Complications of Panreatitis
ii) What is a pancreatic pseudocyst
iii) Complications of chronic pancreatitis
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
Pancreas Function
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
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?
i) CO2 + H20 <–> HCO3- + H+
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
i) DDx for a cool/painful leg
ii) Causes of embolus
iii) Where do emboli tend to get stuck?
iv) Investigations for ALI?
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
Acute Assessment of Sick Patient (CCRISP)
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
Acute Limb Ischaemia Classification
I + IIa - May have time for imaging
IIb + III - Probably not time for imaging
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What consitutes SIRS:
2 or more of:
Temp >38 / <36
RR >20 / PaCO2 <4.3
Pulse >90
WCC > 11 / <4
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
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
Hypoxic Patient:
i) Initial Investigations
ii) Define ARDS
iii) Causes of ARDS
iv ) Management of ARDS
v) Mortality
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%
Present This
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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?
AIrway:
i) Indications for surgical airway
ii) Location of cricothyroidotomy
iii) Location of tracheostomy
i) Indications for surgical airway - Failed intubation + Laryngeal Trauma
ii) Cricothyroidotomy - Through cricothyroid membrane/ligmanet
iii) Tracheostomy - Through the 2nd - 5th Tracheal Rings
Which layers do you traverse when creating a tracheostomy?
Skin
Subcutaenous Fat
Fascia + Platysma
Investing layer of deep cervical fascia
Pretracheal Fascia
Infrahyoid Strap Muscles (retracted)
Thyroid Isthmus
Trachea
i) Consequences of poor pain management
ii) Gross description of pain pathway
iii) Indications for PCA (another card somewhere too) - Dosing
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
Risk factors for chronic post surgical pain
Pre operative pain
Chemotherapy
Long Surgery
Severe post operative pain
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?
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.
Alternatives to blood in Jehova’s Witness
Fluids
Pharmacology - Fe+, EPO, TXA, Factor VIIa
Blood - Autologous, Cell Saver
Intraoperative - Haemostasis, Monitoring and optomisation of homeostasis
- *Brainstem Death:
i) Reversible Causes of coma?**
ii) Who assesses for brainstem death?
iii) Examination?
iv) Absolute/Relative CIs to organ donation
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
Types of ventilation
Supplementary - NC, Venturi, non re breathe, adjuncts
Non invasive - BiPAP, CPAP, Optiflow
Invasive - ET, Trachy
Burns Classification
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i) Criteria for admission to specialist burns unit
ii) Particulars of Hydrofluoric Acid Burns
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
Central Line:
i) Indications
ii) Complications
iii) Insertion Guidelines
iv) IJV Surface Marking
v) Describe procedure - IJV + SCV
vI) Removal
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
Which layers do you pass through to insert a subclavian line?
Skin
Subcut Fat + Fascia
Pec Major
Subclavius Muscle
Subclavian Vein
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?
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
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i) Describe a CVP Trace
ii) Causes of increased/decreased CVP
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,
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Outline ATLS appraoch
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
Describe
![](https://s3.amazonaws.com/brainscape-prod/system/cm/299/282/894/q_image_thumb.png?1578437111)
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
i) Causes of rhabdomyolysis
ii) Lab Testing
iii) Complications
iv) Management
v) Myoglobin vs Haemoglobin in terms of oxygen dissociation
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
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
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)
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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
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
i) Define: DIC
ii) Why is the D Dimer raised in DIC?
iii) List causes of DIC
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
Hypothermia:
i) Definition
ii) Consequences
iii) Intraoperative causes
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
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
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)
Petechial rash over fat, neck and axillae
i) Features
ii) Causes
iii) Pathophysiology
iv) Mode of death
v) Test Results
vi) Mx
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
i) Define : Fistula
ii) Define: Sinus
iii) Define: Abscess
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
Fistulae:
i) Causes of Enterocutaneous Fistula
ii) Classifying Fistulae
iii) Complications of high output fistulae
iv) Enterocutaneous Fistula Management
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
i) What prevents spontaneous healing of fistulae?
ii) Imaging modalities for fistulae
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
i) Normal Calorific Requirements
ii) Calorific Requirements in extensive trauma patients
iii) Caveats in critically ill patients?
iv) Complications of TPN
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
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?
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
i) What specifics do you look for when assessing head injury?
ii) Preventing secondary brain injury
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
- Ventilate to PO2 >13 / PCO2 <5.3 (decreases Cerebral Perfusion Pressure
- Head up position on bed
- Osmotic Diuresis (Mannitol/ Hypertonic Saline
- invasive monitoring - central line/art line/ ICP monitoring
- Extras - Dex, Antibiotics, Fluids, Vasopressors
Hydrocephalus:
i) Definition
ii) Causes
iii) Describe production and circulation of CSF
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
Types of hypersensitivity reaction
+ ?Type V - Formulation of stimulatory antibodies
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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?
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)
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?
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
Levels of care
0 - Ward Care
1 - Ward Care with CCOT input
2 - HDU. One Failing System/ Major Surgery
3 - ITU. >1 Failing System / Advanced monitoring.
i) Indications for tracheostomy
ii) Types of trachy
iii) Types trachy tubing
iv) Complications of Trachy
v) What constitutes trachy care
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
Causes of hyponatraemia
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
i) Causes of SIADH:
ii) Rx
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
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J Osborn Waves - Seen in hypothermia (<32 degrees)
Upward deflection between QRS and ST Segment
Clostridium Tetani:
i) Describe
ii) When are you fully vaccinatd?
iii) Exotoxin vs endotoxin?
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
WRT MODS:
i) What is it?
ii) Which organs can fail?
i) Multi-Organ Dysfunction Syndrome
ii) Renal Failure, Intestinal Failure, Cardiovascular Compromise, Liver Failure, Bone Marrow Failure, Respiratory Failure
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?
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
i) Distribution of water
ii) How much water in the 70 kg man?
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)
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
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
i) Calculation of Minute Ventilation
ii) Complications of mechanical ventilation
iii) When to consider ventilation wean
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)
i) Risk Factors for development of acute AF after surgery
ii) Mx of Acute new onset AF
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
i) Open AAA repair complications
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
Causes of ischaemia
Arterial Occlusion
Venous Congestion
Hypoxia - Pulmonary/ Anaemia/ Carbon monoxide poisoning
Impaired tissue oxygenation due to impaired oxygen dissociation