Anesthesia Pearls

Pearl 10 of 25: Aortocaval Compression in Pregnancy

1. From 20 weeks gestation, gravid uterus compresses the inferior vena cava (IVC) and aorta in supine position.
2. IVC compression: reduces venous return by 25-40% → reduces cardiac output → supine hypotensive syndrome (10-15% of pregnant women symptomatic at term).
3. Aortic compression: reduces uteroplacental blood flow → fetal distress, bradycardia, acidosis. Fetus can be in distress even when maternal BP is maintained (by reflex vasoconstriction).
4. MANDATORY intervention: left lateral tilt of 15° (wedge under right hip or table tilt) in ALL pregnant patients >20 weeks in supine position.
5. Manual uterine displacement (MUD): during LSCS, surgeon displaces uterus manually to left. More effective than wedge in established compression.
6. Supine hypotensive syndrome: pallor, nausea, sweating, hypotension, bradycardia in supine position. Immediate treatment: left lateral tilt → rapid resolution.
7. During CPR in pregnancy: LEFT LATERAL TILT or manual uterine displacement DURING chest compressions. Standard CPR is less effective in supine pregnant patients.
8. Perimortem caesarean section: if cardiac arrest in >20 weeks pregnancy not responding to CPR in 4 minutes → deliver baby by caesarean within 5 minutes. Relieves aortocaval compression → improves CPR effectiveness.
9. IVC compression occurs even in lateral tilt: 15° tilt reduces but does not eliminate compression. In emergency, full left lateral may be needed.
10. Effect on spinal hypotension: aortocaval compression greatly worsens spinal-induced hypotension. Combined: sympathetic block (spinal) + IVC compression = severe hypotension in 80%+ without treatment.
11. Venous return during labour: strong Valsalva during pushing temporarily relieves IVC compression → BP transiently rises then drops with relaxation.
12. Epidural vs spinal in labour: epidural (gradual sympathectomy) better tolerated. Spinal (rapid sympathectomy) in already compressed patient → more severe hypotension.
13. Positioning during intubation: left lateral tilt maintained. Airway assessment while tilted — may make laryngoscopy marginally harder but safety paramount.
14. CTG monitoring: fetal heart rate decelerations with maternal position changes = sign of aortocaval compression. Reposition mother immediately.
15. GA induction: maintain tilt. Vasopressors drawn up and ready before induction. Phenylephrine infusion started simultaneously with spinal injection (most effective prevention).

Pearl 11 of 25: Venous Air Embolism — Detection and Management

1. Venous air embolism (VAE): entry of air (or other gas) into venous system. Causes: open venous channels at surgical site above heart level, CVP line insertion/removal, laparoscopy (CO2 embolism), neurosurgery (sitting position — highest risk).
2. Sitting position: 25-45% incidence VAE in posterior fossa surgery. Head above heart → negative venous pressure at surgical site → air entrainment through open veins.
3. Pathophysiology: air accumulates in RV → 'air lock' → obstruction to pulmonary outflow → acute right heart failure → cardiovascular collapse. Small amounts: V/Q mismatch → hypoxia.
4. Paradoxical embolism: air crosses patent foramen ovale (PFO present in 25-30% of population) → arterial circulation → cerebral, coronary air embolism. Screen for PFO pre-operatively in sitting cases.
5. Monitoring (in order of sensitivity): Transoesophageal Doppler (most sensitive — detects 0.1 mL air), precordial Doppler, end-tidal CO2 (falls when embolism occurs), EtN2 (nitrogen appears if room air entrains), ETCO2/EtN2 ratio, PA catheter (CVP rises), SpO2 (late sign).
6. Clinical features: sudden fall in EtCO2, mill-wheel murmur (churning sound on precordial auscultation), hypotension, dysrhythmias, rising CVP, cyanosis, cardiac arrest.
7. Mill-wheel murmur: pathognomonic — loud churning murmur audible with stethoscope on chest when large amount of air in heart. Late sign — significant VAE.
8. Immediate management: (1) Flood surgical field with saline/pack wound. (2) Inform surgeon — stop the source. (3) Place patient head-down + left lateral (Durant manoeuvre — air to RV apex away from outflow). (4) 100% oxygen (speeds nitrogen reabsorption). (5) Stop N2O immediately (expands air bubble). (6) Aspirate via central venous catheter (right heart). (7) CPR if arrest.
9. Durant manoeuvre: left lateral decubitus (left side down) + Trendelenburg (head down). Moves air bubble from RV outflow tract to RV apex — prevents outflow obstruction.
10. Aspiration: multi-orifice CVP catheter positioned in right atrium can aspirate air. Most effective when large air lock. Aspirate while performing CPR.
11. N2O: IMMEDIATELY discontinue. N2O is 34x more soluble than nitrogen — diffuses into air bubble rapidly, expanding it. Can convert subclinical embolism to fatal one.
12. CO2 embolism (laparoscopy): less severe — CO2 absorbed 20x faster than nitrogen. Treatment same as air but expected to resolve faster with good supportive care.
13. Prevention in sitting position: maintain MAP ≥70 mmHg (reduces venous negative pressure gradient), careful surgical technique (bone wax, bipolar for bleeding), PEEP 5-10 cmH2O controversial (may worsen paradoxical embolism).
14. EtCO2 monitoring: non-specific but very sensitive. Fall >3 mmHg from baseline → suspect VAE. Combined with precordial Doppler = standard monitoring for sitting position cases.
15. Hyperbaric oxygen (HBO): for paradoxical arterial embolism causing neurological deficit. Reduces bubble size, treats cerebral air embolism. Transfer to HBO chamber if available.

Pearl 12 of 25: Bone Cement Implantation Syndrome (BCIS)

1. Definition: syndrome occurring during/after cementing of prostheses in orthopaedic surgery (THR, TKR, femoral nailing). Features: hypoxia, hypotension, loss of consciousness, cardiac arrest.
2. Mechanism: pressurising cement into medullary canal forces fat, marrow, air, bone particles, cement monomers into venous sinusoids → pulmonary embolism + fat embolism. Also: methyl methacrylate (MMA) monomer causes vasodilation and myocardial depression.
3. BCIS Grading (Donaldson): Grade 1 — SpO2 <94% OR hypotension (>20% MAP fall); Grade 2 — SpO2 <88% OR >40% MAP fall or unexpected LOC; Grade 3 — cardiovascular collapse requiring CPR.
4. Timing: symptoms typically occur within 60-90 seconds of cement insertion and pressurisation. Maximum risk during femoral canal reaming and cement pressurisation.
5. Risk factors for BCIS: elderly, osteoporosis, pathological fractures (metastatic bone), long stem prostheses, previous cemented arthroplasty, pulmonary hypertension, cardiac disease.
6. High-risk patients: pre-operative echo to assess RV function and pulmonary pressures. Consider uncemented prosthesis in very high-risk patients.
7. Haemodynamic changes: transient rise in CVP (RV overload), fall in MAP, fall in EtCO2 (pulmonary emboli — dead space), fall in SpO2 (right-to-left shunting + V/Q mismatch).
8. Management: ANTICIPATE. Tell surgeon to slow pressurisation. Increase FiO2 to 1.0 before cementing. IV fluid bolus 250-500 mL before cementing. Vasopressors drawn up and ready.
9. Vasopressors: phenylephrine/noradrenaline for hypotension. Adrenaline for severe cardiovascular collapse. CPR if cardiac arrest.
10. Pre-treatment with vasopressors: some anaesthetists give phenylephrine 100 mcg IV prophylactically before cementing in high-risk patients. Evidence limited but logical.
11. General vs regional: regional anaesthesia may not prevent BCIS but haemodynamic response may differ. No clear evidence one technique is superior in high-risk.
12. Irrigation of medullary canal: using pulsatile lavage before cementing reduces fat/marrow load. Reduces BCIS incidence.
13. Fat embolism syndrome vs BCIS: BCIS is acute (intraoperative). Fat embolism syndrome typically delayed 24-72 hours. Both have fat and marrow emboli in pathophysiology.
14. Monitoring: continuous SpO2, EtCO2 (fall during cementing = emboli), arterial line for high-risk cases, CVP (rises with RV strain).
15. Prognosis: Grade 3 BCIS has 20-30% mortality. Early recognition and aggressive management critical. Post-op HDU/ICU for high-grade BCIS.

Pearl 13 of 25: Perioperative Myocardial Injury (MINS) and Troponin Monitoring

1. MINS (Myocardial Injury after Non-cardiac Surgery): elevation of high-sensitivity troponin T (hsTnT) above 14 ng/L within 30 days of surgery from ischaemic myocardial injury.
2. VISION study (2012, 8,351 patients): MINS occurred in 8% of patients aged >45 years. 30-day mortality was 10x higher in MINS patients vs non-MINS (9.8% vs 1.1%).
3. Distinguish from NSTEMI: MINS does not require symptoms, ECG changes, or imaging evidence. Simply troponin rise + perioperative context + no non-ischaemic cause.
4. Mechanism: most MINS is due to supply-demand mismatch (tachycardia, hypotension, anaemia) rather than plaque rupture (Type 2 MI). Silent in >65% of cases — no chest pain (masked by analgesia).
5. Risk factors: age >65, known cardiac disease, DM, renal failure, vascular disease, emergency surgery, prolonged surgery >2 hours.
6. Screening protocol: hsTnT at 24 and 48 hours post-op in ALL patients >65 years OR any age with known cardiovascular disease undergoing major surgery.
7. Baseline hsTnT: ideally obtain pre-operatively (especially in known cardiac disease). Acute rise (>20% increase) above pre-op baseline is more meaningful than a single post-op reading.
8. Management of detected MINS: (1) Aspirin 100 mg daily. (2) Statin if not already prescribed. (3) ACE inhibitor. (4) Beta-blocker if appropriate. (5) Cardiology referral. (6) Consider anti-platelet escalation.
9. MANAGE trial (2018): Dabigatran (direct thrombin inhibitor) significantly reduced major vascular events (MI, stroke, PE) after MINS diagnosis (hazard ratio 0.72).
10. Type 1 MI vs Type 2 MI vs MINS: Type 1 = plaque rupture + thrombus. Type 2 = supply-demand mismatch without plaque. MINS = any ischaemic troponin rise perioperatively.
11. ECG: only 35% of MINS patients have ECG changes. ECG alone is NOT adequate screening. Routine post-op ECG misses 65%.
12. Timing: peak troponin usually Day 2-3 post-op (catecholamine surge, hypercoagulable state, pain, mobilisation). Stay vigilant through first week.
13. hsTnT vs conventional troponin: hsTnT detects lower levels, faster, more sensitive. Enables earlier diagnosis and risk stratification.
14. MINS in different surgeries: highest incidence in major vascular (AAA repair), cardiac, major thoracic, and emergency abdominal. Also significant in orthopaedic and major abdominal.
15. Communication with patient: inform about MINS diagnosis, importance of cardiac follow-up, lifestyle modifications, medication adherence. MINS survivors at long-term risk for further cardiac events.

Pearl 14 of 25: Goal-Directed Fluid Therapy (GDFT) — Evidence and Practice

1. Goal-directed fluid therapy (GDFT): using haemodynamic parameters to give IV fluid only when patient is fluid-responsive, rather than fixed-rate formulas.
2. Fluid responsiveness: cardiac output increases ≥10-15% in response to 200-250 mL fluid bolus. If non-responsive: further fluid causes only harm (pulmonary oedema, tissue oedema, AKI).
3. Dynamic measures of fluid responsiveness: Pulse Pressure Variation (PPV >13%), Stroke Volume Variation (SVV >13%), Passive Leg Raise (CO increase ≥10%), Oesophageal Doppler (corrected flow time FTc <350 ms), End-expiratory occlusion test.
4. PPV and SVV prerequisites: sinus rhythm essential, controlled ventilation (no spontaneous breaths), tidal volume ≥8 mL/kg IBW, no right heart failure, no open chest.
5. Oesophageal Doppler (Cardio-Q): placed in oesophagus, measures descending aortic blood flow. Corrected flow time (FTc) <350 ms = hypovolaemic. Stroke volume increase >10% after 250 mL fluid = fluid responsive. Non-invasive, good evidence base.
6. GIFTASUP trial (NHS 2011): oesophageal Doppler-guided GDFT reduced hospital stay, complications and cost vs conventional fluid management in GI surgery.
7. OPTIMISE trial (JAMA 2014): GDFT using oesophageal Doppler + cardiac output optimisation trend toward improved outcomes in high-risk surgery.
8. FlowTrac/Vigileo: arterial waveform analysis for continuous SVV and CO. Practical alternative to oesophageal Doppler. Less accurate in arrhythmias and extremes of vascular resistance.
9. Phases of fluid management in surgery: (1) Resuscitation (restore circulating volume). (2) Optimisation (maintain adequate perfusion during surgery). (3) Stabilisation (maintain homeostasis post-op). (4) De-escalation (remove excess fluid).
10. Conservative vs liberal vs GDFT: Liberal fluid associated with: weight gain, pulmonary oedema, delayed GI function, prolonged ICU stay. Restrictive: AKI, hypotension. GDFT: individualised, best outcomes.
11. RELIEF trial (NEJM 2018): restrictive vs liberal fluid strategy in abdominal surgery. Restrictive associated with higher AKI and 1-year disability in some analyses — not definitively better.
12. METS trial: neither liberal nor restricted fluid strategy superior. GDFT personalised approach most logical.
13. Fluid bolus administration: give as a BOLUS (200-250 mL over 5-10 minutes), not continuous infusion. Assess response. Repeat only if still fluid responsive.
14. Vasopressor threshold: if MAP <65 despite adequate volume: ADD vasopressor. Do not give more fluid hoping it raises BP if patient is non-responsive (fluid overload).
15. GDFT in ERAS: fundamental component of ERAS protocols. Near-zero balance intraoperatively for elective cases. Reduces ileus, complications, LOS. Active fluid removal post-op (SSC 2024 — sepsis) and ERAS protocols increasingly advocate de-escalation phase.

Pearl 15 of 25: Perioperative Anticoagulation — LMWH, DOACs and Warfarin

1. Hold anticoagulants before surgery: prevents surgical haemorrhage. Resume as soon as haemostasis established: prevents thromboembolism.
2. Warfarin: Stop 5 days before surgery. Check INR day before. If INR >1.5: give vitamin K 1-2 mg orally. For emergency surgery: Prothrombin Complex Concentrate (PCC 25 IU/kg) + Vitamin K 5 mg IV. Resume warfarin evening of surgery or next day.
3. LMWH (enoxaparin, dalteparin): prophylactic dose — stop 12 hours before. Therapeutic dose — stop 24 hours before. No routine monitoring needed (anti-Xa level if renal impairment). Resume 12-24 hours post-op.
4. Unfractionated heparin (UFH) infusion: stop 4-6 hours before. Check APTT. Can reverse with protamine 1 mg per 100 units heparin given in last 4 hours.
5. Direct Oral Anticoagulants (DOACs): Dabigatran (direct thrombin inhibitor), Rivaroxaban/Apixaban/Edoxaban (Factor Xa inhibitors).
6. DOAC stopping times (based on renal function): Normal renal function: Dabigatran stop 48h (24h for low-risk surgery); Rivaroxaban/Apixaban stop 24h (12h low-risk). Renal impairment: extend by 24-48 hours (dabigatran predominantly renally excreted).
7. DOAC reversal: Dabigatran → Idarucizumab (Praxbind) 5g IV. Rivaroxaban/Apixaban → Andexanet alfa (Ondexxya). Both reverse within minutes. OR PCC 25-50 IU/kg if reversal agents unavailable.
8. Bridging therapy: historically LMWH bridging used for high-risk patients (mechanical heart valves, AF with high CHA2DS2-VASc, recent VTE). BRIDGE trial (2015): bridging NOT superior to stopping warfarin alone for most AF patients — increased bleeding. Bridging now reserved for mechanical mitral valves and recent (within 3 months) VTE.
9. Antiplatelet agents: Aspirin — continue for most surgery (cardiac risk outweighs bleeding). DAPT (aspirin + clopidogrel/ticagrelor): after DES minimum 6 months, after BMS 1 month — do NOT stop without cardiologist consultation.
10. P2Y12 inhibitors: clopidogrel — stop 5-7 days. Ticagrelor — stop 5 days. Prasugrel — stop 7 days. If emergency surgery during DAPT: accept increased bleeding risk or discuss with cardiologist about surgical vs percutaneous approach.
11. Heparin-induced thrombocytopenia (HIT): platelet fall >50% or <100,000 after 5-10 days of heparin. Paradoxically thrombotic (not bleeding). Stop ALL heparin immediately. Use alternative anticoagulant (fondaparinux, argatroban, bivalirudin). 4T score for diagnosis.
12. Spinal/epidural with anticoagulation: ASRA 2018 guidelines. LMWH prophylactic: 12 hours before, 12 hours after catheter removal. Therapeutic LMWH: 24 hours before. DOACs: specific timings. Warfarin: INR <1.5. These guidelines prevent epidural haematoma.
13. Anti-Xa levels: monitoring for LMWH (especially renal impairment, obesity, pregnancy). Peak anti-Xa 4 hours after dose: prophylactic 0.2-0.5 IU/mL, therapeutic 0.5-1 IU/mL.
14. Aspirin mechanism: irreversibly inhibits COX-1 → blocks TXA2 → platelet aggregation impaired for the platelet's lifetime (7-10 days). Single aspirin affects platelets permanently. 80% of platelet mass can turn over in 5 days — by day 5 after stopping, platelet function largely restored.

Pearl 16 of 25: Thromboelastogram (TEG) and Viscoelastic Testing

1. Thromboelastography (TEG) and Rotational Thromboelastometry (ROTEM) are whole-blood assays measuring the ENTIRE coagulation process from clot formation to lysis in 10-20 minutes.
2. Conventional coagulation tests (PT/INR, aPTT, platelets) take 45-60 minutes, measure only plasma factors in isolation — miss platelet function, fibrinolysis, clot strength. Useless for real-time management of massive haemorrhage.
3. TEG measures: R-time (reaction time = time to first fibrin formation), K-time (clot formation time), Alpha angle (rate of clot strengthening), MA (maximum amplitude = clot strength), LY30 (% lysis at 30 minutes).
4. ROTEM equivalent parameters: CT (clotting time ≈ R-time), CFT (clot formation time ≈ K-time), Alpha angle, A10/A20/MCF (maximum clot firmness ≈ MA), LI30 (lysis index).
5. TEG/ROTEM interpretation: R-time/CT prolonged → factor deficiency → give FFP or PCC. MA/MCF reduced → poor platelet function → give platelets. Fibrin clot strength (FIBTEM) low → hypofibrinogenaemia → give cryoprecipitate or fibrinogen concentrate. High lysis (LY30 >3% or LI60 <85%) → fibrinolysis → give TXA.
6. ROTEM channels: EXTEM (extrinsic pathway, overall coagulation), INTEM (intrinsic pathway), FIBTEM (fibrin-specific — without platelets, shows fibrinogen contribution), HEPTEM (neutralises heparin for cardiac bypass patients), APTEM (detects fibrinolysis).
7. Fibrinogen first: Clauss fibrinogen from FIBTEM A10 guides fibrinogen concentrate dosing. Target fibrinogen >2 g/L. Fibrinogen is the FIRST coagulation protein to fall critically in massive haemorrhage.
8. ITACTIC trial (NEJM 2020): TEG/ROTEM guided MTP vs conventional laboratory guided MTP — no difference in 28-day mortality or 24-hour blood product use. Both strategies effective. TEG/ROTEM faster and more practical.
9. Platelet function: MA on TEG reflects combined platelet + fibrinogen contribution. ROTEM FIBTEM removes platelet contribution — low FIBTEM A10 with low EXTEM A10 = fibrinogen problem. Low EXTEM A10 with normal FIBTEM A10 = platelet problem.
10. TEG and antiplatelet therapy: TEGplate assay detects residual aspirin and clopidogrel effect on platelets. Guides when to proceed with regional anaesthesia or surgery in patients on antiplatelet drugs.
11. Heparin monitoring: ROTEM HEPTEM: reversal of heparin in the assay. If INTEM CT normalises with HEPTEM = heparin present. If both prolonged = factor deficiency.
12. Cardiac surgery application: standard of care for haemorrhage management after cardiopulmonary bypass. Post-bypass coagulopathy is complex — TEG/ROTEM differentiates causes and guides targeted product transfusion.
13. Liver transplantation: complex coagulopathy throughout. TEG guides product administration at different stages (anhepatic phase, reperfusion). Traditional tests unreliable in liver disease.
14. Obstetric haemorrhage: ROTEM rapidly identifies coagulopathy in PPH. Fibrinogen <2 g/L (FIBTEM MCF <12 mm) = give fibrinogen concentrate. Faster than conventional tests for decision-making.
15. Cost-effectiveness: TEG/ROTEM guided therapy reduces blood product use and transfusion-related complications in cardiac, liver, and trauma settings. Cost of device offset by savings in blood products.

Pearl 17 of 25: Uterine Atony and Obstetric Haemorrhage

1. Primary PPH (Postpartum Haemorrhage): blood loss ≥500 mL within 24 hours of vaginal delivery, or ≥1000 mL after caesarean section. Severe PPH: >1000 mL with signs of shock.
2. 4Ts mnemonic for PPH causes: Tone (uterine atony — 70-80%), Trauma (lacerations, uterine rupture), Tissue (retained placenta, membranes, clots), Thrombin (coagulopathy — DIC, inherited disorders).
3. Uterine atony: failure of uterus to contract after delivery. Risk factors: high parity, multiple pregnancy, polyhydramnios, prolonged labour, augmented labour, placenta praevia, macrosomia, chorioamnionitis, previous PPH.
4. First-line treatment: bimanual uterine compression + oxytocin 5-10 IU IV slow bolus (NEVER rapid bolus — causes hypotension, dysrhythmia) + oxytocin infusion 20-40 IU in 1 litre over 4 hours.
5. Second-line uterotonics: Ergometrine 500 mcg IM (not IV — hypertension, vomiting). Carboprost (15-methyl PGF2α) 250 mcg IM every 15 minutes (max 8 doses). AVOID ergometrine in hypertension, cardiac disease.
6. Carbetocin: long-acting oxytocin analogue. 100 mcg IV single dose at LSCS — evidence shows similar efficacy to oxytocin infusion with single dose convenience. WHO recommends for elective LSCS.
7. Misoprostol: 800 mcg sublingual or rectal. Useful in resource-limited settings (no refrigeration needed). Cheaper but more side effects (shivering, fever).
8. Tranexamic acid (TXA): WOMAN trial (2017): TXA 1g IV within 3 hours of delivery reduces death from haemorrhage in PPH (relative risk 0.81). WHO recommends TXA for ALL PPH regardless of cause.
9. Massive PPH resuscitation: 1:1:1 FFP:Platelets:PRBCs (same as trauma). TXA 1g IV immediately. Calcium gluconate 1g IV q4 units blood. Fibrinogen >2 g/L target (ROTEM/TEG guided if available).
10. Surgical options (stepwise): balloon tamponade (SOS Bakri balloon) → B-Lynch compression suture → uterine artery ligation → internal iliac artery ligation → hysterectomy (last resort, life-saving).
11. Interventional radiology: uterine artery embolisation (UAE) — effective for atony, placenta praevia/accreta. Requires: haemodynamically stable patient, IR suite availability.
12. Placenta accreta spectrum (PAS): abnormal placental invasion (accreta, increta, percreta). Catastrophic haemorrhage risk at delivery. Risk factors: previous CS + anterior placenta praevia. Management: planned preterm LSCS by specialist team, cell salvage available, balloon catheters pre-placed, massive transfusion protocol activated.
13. Cell salvage: acceptable in obstetrics (RCOG 2015) — leucocyte depletion filter used to remove fetal cells. Does NOT increase risk of fetal sensitisation or maternal complications.
14. Anaesthetic role in PPH: provide large bore IV access (x2), arterial line for haemodynamic instability, cross-match 6 units, activate MTP early, maintain normothermia, correct coagulopathy, vasopressors (noradrenaline preferred), communicate clearly with obstetric team.
15. HAEMOSTASIS acronym for PPH management: H-ask for Help, A-Assess and resuscitate, E-Establish cause, M-Massage uterus, O-Oxytocics, S-Shift to OT, T-Tamponade, A-Apply pressure sutures, S-Systematic pelvic devascularisation, I-Interventional radiology, S-Subtotal/total hysterectomy.

Pearl 18 of 25: Non-Invasive Cardiac Output Monitoring

1. Non-invasive cardiac output monitoring (NICOM) avoids complications of PA catheter (pneumothorax, haematoma, arrhythmia, PA rupture, sepsis) while providing haemodynamic data.
2. Oesophageal Doppler (CardioQ): inserts nasogastrically. Measures blood flow velocity in descending thoracic aorta using pulsed-wave Doppler. Calculates stroke volume, CO, corrected flow time (FTc). Best validated non-invasive CO device. Evidence base: multiple RCTs show reduced complications and LOS with GDFT using oesophageal Doppler.
3. FTc (corrected flow time): normal 330-360 ms. <330 ms = hypovolaemia (shorter systolic ejection = less filling). Fluid bolus if low + patient fluid-responsive.
4. LiDCO (Lithium dilution cardiac output): transpulmonary lithium dilution calibrated technique. Accurate, minimally invasive (peripheral IV + arterial line). Continuous SV and CO thereafter by waveform analysis. Calibration required periodically.
5. PiCCO (Pulse Contour Cardiac Output): transpulmonary thermodilution calibration (cold saline via central line). Provides: CO, SVV, Extravascular Lung Water (EVLW), Global End-Diastolic Volume (GEDV). EVLW >10 mL/kg = pulmonary oedema. Requires femoral or brachial arterial line.
6. Vigileo/FloTrac: uncalibrated arterial waveform analysis. Continuous CO and SVV from radial A-line alone. No calibration injection needed. Less accurate in extreme vasoplegia or vasoconstriction, significant aortic regurgitation.
7. USCOM (Ultrasonic Cardiac Output Monitor): Doppler-based probe placed on chest wall or suprasternal notch. Non-invasive, no insertion required. Accuracy lower than oesophageal Doppler but useful for spot measurements.
8. Bioreactance (NICOM, Cheetah Medical): four electrodes applied to chest measure thoracic bioreactance changes with each heartbeat. Truly non-invasive CO estimate. Less accurate but trending useful.
9. Pulse oximetry plethysmography variability index (PVI): variation in pulse oximeter waveform amplitude with respiration. >14% = fluid responsive. Non-invasive alternative to PPV when A-line not available.
10. Near-infrared spectroscopy (NIRS/rSO2): cerebral oximetry (INVOS, ForeSight). Measures cerebral O2 saturation. Fall >20% from baseline or absolute <50% = intervention needed. Used in cardiac surgery, carotid endarterectomy, beach chair position.
11. Transthoracic echocardiography (TTE): non-invasive, bedside. POCUS (Point of Care Ultrasound) — rapidly assess cardiac function, LV filling, RV function, pericardial effusion, IVC collapsibility. PLAX, PSAX, A4C, subcostal views.
12. IVC collapsibility index: IVC diameter varies with respiration in spontaneously breathing patients. >50% collapse = fluid responsive. <50% collapse = adequate filling. Less reliable in controlled ventilation.
13. Bioimpedance/bio-electrical impedance: thoracic electrical bioimpedance changes with aortic blood velocity. Non-invasive but poor accuracy in pacemakers, arrhythmias, fluid overload.
14. CPET (cardiopulmonary exercise testing): gold standard for cardiac reserve assessment. VO2 max >20 mL/kg/min = good reserve. <10 mL/kg/min = very high-risk. Used preoperatively for major surgery risk stratification.
15. Clinical application guide: routine major elective surgery → oesophageal Doppler or FloTrac. Cardiac surgery/critical care → PiCCO or PA catheter. Emergency quick assessment → TTE/POCUS. Pre-op high-risk assessment → CPET. Paediatric ICU → oesophageal Doppler or PRAM.

Pearl 19 of 25: Fat Embolism Syndrome — Diagnosis and Management

1. Fat embolism syndrome (FES): systemic manifestation of fat emboli lodging in pulmonary vasculature and microcirculation. Distinct from BCIS (intraoperative) — FES is subacute (12-72 hours after injury).
2. Causes: long bone fractures (femur, tibia — highest risk), pelvis fractures, bilateral femoral reaming, liposuction, bone marrow transplant, pancreatitis, sickle cell crisis, CPR, closed chest cardiac massage.
3. Classic triad (Gurd's criteria): (1) Respiratory — hypoxia, tachypnoea, ARDS pattern on CXR. (2) Neurological — confusion, agitation, focal deficits, reduced GCS (cerebral fat emboli). (3) Petechial rash — axillae, chest, conjunctivae (50-60% of cases — pathognomonic when present).
4. Petechial rash: appears 24-36 hours after injury. Caused by fat emboli in skin capillaries with platelet activation. Transient — may resolve in 24 hours. Check axillae, subconjunctival areas — easily missed.
5. Pathophysiology: two theories — (1) Mechanical: fat globules from marrow enter venous sinusoids at fracture site → pulmonary capillaries → obstruction → V/Q mismatch. (2) Biochemical: lipase breaks fat down to free fatty acids → endothelial toxicity → inflammatory response → ARDS-like picture.
6. Gurd's diagnostic criteria — MAJOR features (1 required): petechiae, respiratory insufficiency (PaO2 <60), neurological symptoms. MINOR features (at least 4): tachycardia >110, pyrexia, fat in urine/sputum, thrombocytopenia, anaemia (Hb fall >2g/dL), high ESR, fat globules on fundoscopy.
7. Lab findings: fat globules in urine (lipaemia), thrombocytopenia, fat droplets in BAL (bronchoscopy), elevated lipase, elevated ESR, coagulopathy. None are pathognomonic — diagnosis clinical.
8. MRI brain: most sensitive imaging. Shows multiple petechial lesions in white matter (star field pattern) from cerebral fat emboli. CT brain: less sensitive but rules out other causes.
9. CXR/HRCT chest: bilateral interstitial infiltrates (snowstorm pattern) — non-specific ARDS pattern. Develops 24-48 hours after injury.
10. Prevention: early fracture fixation (<24 hours) reduces fat embolism. Intramedullary reaming technique — vented reamer. Prophylactic steroids (controversial) — some evidence for prevention.
11. Steroids: methylprednisolone 6 mg/kg/day in 3 divided doses — some evidence for prevention in high-risk patients (bilateral femoral fractures). NOT recommended for treatment once established.
12. Treatment: supportive. O2/mechanical ventilation for ARDS (lung-protective: 6 mL/kg IBW, PEEP 5-10). Haemodynamic support. Heparin: promotes lipase activity — theoretical but not proven. Alcohol: inhibits lipase — historical, abandoned.
13. Prognosis: most cases mild and self-limiting. Severe FES with ARDS: mortality 10-20%. Full neurological recovery possible even in severe cerebral involvement.
14. Alcohol and FES: interestingly, moderate alcohol may reduce FES risk — alcohol inhibits lipase, reducing free fatty acid generation. This is a pharmacological curiosity, not a recommendation.
15. Timing of surgery after FES: typically wait 48-72 hours for mild cases. If fracture not yet fixed: haematology/orthopaedic MDT decision based on physiological stability.