Membership of the Royal College of Surgeons (MRCS) Perioperative Care and Critical Care Flashcards

24 sample cards from the Perioperative Care and Critical Care deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. State the Parkland formula for fluid resuscitation in major burns.

   $$\text{Total fluid (mL in 24h)} = 4 \times \text{weight (kg)} \times \%\ \text{TBSA burned}$$ Give half in the first 8 hours from the time of injury and the remaining half over the next 16 hours, using Hartmann's solution; titrate to urine output ($0.5$–$1\ \text{mL/kg/h}$).

2. What are the daily maintenance requirements for water, sodium and potassium in an adult per NICE IV fluid guidance?

   Water $25$–$30\ \text{mL/kg/day}$; sodium, potassium and chloride approximately $1\ \text{mmol/kg/day}$ each; and glucose $50$–$100\ \text{g/day}$ to limit ketosis.

3. Compare the composition of 0.9% saline and Hartmann's solution, and the main drawback of large-volume saline.

   0.9% saline: $\text{Na}^+\ 154$, $\text{Cl}^-\ 154\ \text{mmol/L}$. Hartmann's (compound sodium lactate): $\text{Na}^+\ 131$, $\text{Cl}^-\ 111$, $\text{K}^+\ 5$, $\text{Ca}^{2+}\ 2$, lactate $29\ \text{mmol/L}$. Large-volume saline causes hyperchloraemic metabolic acidosis, so balanced crystalloids are preferred.

4. What is refeeding syndrome, the key biochemical abnormality, and who is at risk?

   A dangerous fluid/electrolyte shift on reintroducing nutrition to a starved patient, driven by an insulin surge. The hallmark is hypophosphataemia (also hypokalaemia, hypomagnesaemia and thiamine deficiency), risking arrhythmias and cardiac failure. High risk: $BMI < 16$, $>15\%$ weight loss, or little intake for $>10$ days.

5. When is parenteral nutrition indicated over enteral nutrition, and what is the guiding principle?

   Principle: 'if the gut works, use it' — enteral feeding is preferred (maintains gut integrity, fewer infections). Parenteral nutrition is indicated when the GI tract is non-functional, inaccessible or unsafe: intestinal failure, high-output fistula, prolonged ileus, short bowel, or severe malabsorption.

6. Differentiate an open versus closed surgical drain and give an example of each.

   Open drains (e.g. corrugated/Penrose drain) drain into a dressing or stoma bag, allowing free drainage but higher infection risk. Closed drains (e.g. Redivac suction drain, chest drain) connect to a sealed system, reducing infection and allowing measurement; they may be active (suction) or passive (gravity).

7. How do you distinguish an end colostomy from a loop ileostomy on examination?

   Colostomy: usually in the left iliac fossa, flush to skin, with formed/solid faecal output. Ileostomy: usually in the right iliac fossa, spouted (to protect skin from enzymatic effluent), with loose/liquid output. A loop stoma has two openings (afferent and efferent limbs) over a bridge/rod.

8. What is the SOFA score and which six organ systems does it assess?

   The Sequential Organ Failure Assessment score quantifies multi-organ dysfunction (0–4 points per system). The six systems: respiratory ($P_aO_2/F_iO_2$), coagulation (platelets), liver (bilirubin), cardiovascular (MAP/vasopressors), CNS (Glasgow Coma Scale), and renal (creatinine/urine output).

9. Define MODS (multi-organ dysfunction syndrome) and name the proposed mechanisms.

   MODS is the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention, typically affecting $\geq 2$ systems. Mechanisms: uncontrolled systemic inflammation (SIRS), tissue hypoxia/microcirculatory failure, gut barrier failure with bacterial translocation, and apoptosis.

10. State the Berlin definition criteria for Acute Respiratory Distress Syndrome (ARDS) and its severity grading.

    ARDS: acute onset within 1 week, bilateral infiltrates on imaging not fully explained by cardiac failure/fluid overload, and hypoxaemia with PEEP $\geq 5\ \text{cmH}_2\text{O}$. Severity by $P_aO_2/F_iO_2$ ratio: mild $201$–$300$, moderate $101$–$200$, severe $\leq 100\ \text{mmHg}$.

11. What lung-protective ventilation strategy is used in ARDS?

    Low tidal volume of $6\ \text{mL/kg}$ predicted body weight, plateau pressure $<30\ \text{cmH}_2\text{O}$, permissive hypercapnia, appropriate PEEP, and prone positioning for severe cases ($P_aO_2/F_iO_2 < 150$).

12. Define acute kidney injury (AKI) using the KDIGO criteria.

    AKI is defined by any of: a rise in serum creatinine $\geq 26\ \mu mol/L$ within 48 hours; a rise to $\geq 1.5\times$ baseline within 7 days; or urine output $<0.5\ \text{mL/kg/h}$ for $>6$ hours. Stages 1–3 grade severity by the magnitude of creatinine rise and oliguria.

13. List the emergency indications for renal replacement therapy (dialysis) — the 'AEIOU' mnemonic.

    Acidosis (severe metabolic, $pH < 7.1$ refractory), Electrolytes (refractory hyperkalaemia $>6.5\ \text{mmol/L}$), Intoxication (dialysable toxins, e.g. lithium, salicylates), Overload (refractory pulmonary oedema), and Uraemia (pericarditis, encephalopathy).

14. What is the lethal triad (trauma triad of death) in perioperative bleeding management?

    Hypothermia, acidosis and coagulopathy — a self-perpetuating vicious cycle. Hypothermia and acidosis impair clotting enzyme function and platelet activity, worsening haemorrhage, which deepens shock and acidosis. Breaking the cycle is central to damage control resuscitation.

15. Define damage control resuscitation and its key components.

    An approach for the exsanguinating patient combining: permissive hypotension (target $SBP$ ~$80$–$90\ \text{mmHg}$ until haemorrhage controlled), haemostatic resuscitation with balanced blood products (~$1{:}1{:}1$ RBC:FFP:platelets), minimal crystalloid, early tranexamic acid, and damage control surgery to rapidly control bleeding and contamination.

16. What is the role and dosing of tranexamic acid (TXA) in major haemorrhage?

    TXA is an antifibrinolytic (lysine analogue) that inhibits plasminogen activation. In trauma (CRASH-2) give $1\ \text{g}$ IV over 10 min then $1\ \text{g}$ over 8 hours, ideally within 3 hours of injury to reduce mortality. Also used in major elective surgery and PPH.

17. Outline the normal coagulation cascade pathways and which tests assess each.

    Intrinsic pathway (factors XII, XI, IX, VIII) is assessed by APTT; extrinsic pathway (factor VII, tissue factor) is assessed by PT/INR; both converge on the common pathway (factors X, V, II/thrombin, I/fibrinogen). Thrombin time and fibrinogen assess the final fibrin step.

18. How does ROTEM/TEG (viscoelastic testing) guide blood product replacement?

    It measures clot formation in real time. A prolonged clotting time (CT/R) suggests need for FFP/clotting factors; reduced clot amplitude/firmness (MCF/MA) with low fibrinogen suggests cryoprecipitate/fibrinogen concentrate; low platelet contribution suggests platelet transfusion; and a high lysis index (LY30/ML) indicates fibrinolysis warranting tranexamic acid.

19. What are the standard transfusion thresholds for red cells, platelets and the target in active bleeding?

    Restrictive RBC threshold: transfuse if $Hb < 70\ \text{g/L}$ (or $<80\ \text{g/L}$ in acute coronary syndrome). Prophylactic platelet threshold $<10 \times 10^9/L$ (higher, $<50$, if bleeding/surgery). In major haemorrhage aim to keep platelets $>50 \times 10^9/L$, fibrinogen $>1.5\ \text{g/L}$ and $PT/APTT$ ratio $<1.5$.

20. Distinguish TACO from TRALI as transfusion complications.

    TACO (transfusion-associated circulatory overload): hydrostatic pulmonary oedema from volume overload, with hypertension, raised JVP/BNP, responds to diuretics. TRALI (transfusion-related acute lung injury): non-cardiogenic pulmonary oedema within 6 hours from donor antibodies/neutrophil activation, with hypotension, normal JVP, normal BNP, managed with supportive ventilation.

21. What metabolic complication arises from massive transfusion and why?

    Citrate (anticoagulant in stored blood) chelates calcium causing hypocalcaemia (and metabolic alkalosis once citrate is metabolised). Also hyperkalaemia (from stored cells), hypothermia (cold products) and dilutional thrombocytopenia/coagulopathy. Monitor and replace ionised calcium and warm products.

22. List the components of Virchow's triad explaining venous thromboembolism.

    1) Venous stasis (immobility, surgery), 2) Endothelial/vessel wall injury (surgical trauma), and 3) Hypercoagulability (malignancy, surgery, thrombophilia, oestrogens). The perioperative period maximises all three, making VTE prophylaxis essential.

23. Outline the mechanical and pharmacological options for VTE prophylaxis in surgical patients.

    Mechanical: anti-embolic (graduated compression) stockings and intermittent pneumatic compression devices (used when bleeding risk is high or anticoagulation contraindicated). Pharmacological: low-molecular-weight heparin (e.g. enoxaparin $40\ \text{mg}$ SC daily), unfractionated heparin (in renal failure), or fondaparinux; early mobilisation and hydration are adjuncts.

24. What scoring tools assess VTE and bleeding risk to guide thromboprophylaxis, and what is the Wells score used for?

    NICE recommends a documented VTE risk assessment (e.g. Department of Health VTE tool) balanced against bleeding risk for every surgical admission. The Wells score is used to estimate the clinical pretest probability of an established DVT or PE (not for prophylaxis), guiding D-dimer testing versus imaging.

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