Anesthesia

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Weaning from Mechanical Ventilation

description Clinical Response

CLINICAL

1	Readiness criteria for weaning: SOAP-ME mnemonic — Spontaneous breathing ability; Oxygenation adequate (FiO₂ ≤0.4–0.5, PEEP ≤5–8 cmH₂O, P/F ≥150–200); Adequate secretion management (cough); Patient awake/cooperative (RASS 0 to −1); Medical stability (no vasopressor escalation, afebrile); Etiology of respiratory failure reversed or improving.
2	Rapid Shallow Breathing Index (RSBI) = RR/VT (L). Measured during 1–2 min spontaneous breathing without support. RSBI <105 predicts successful extubation with ~80% sensitivity/specificity (Yang & Tobin, 1991). RSBI >105 predicts failure. It is a screening tool, not a standalone extubation criterion — clinical context (secretion burden, upper airway patency, neurological status) must accompany RSBI assessment.
3	Spontaneous Breathing Trial (SBT): conduct for 30–120 minutes on T-piece, CPAP 5 cmH₂O, or low-level PSV (5–8 cmH₂O). Failure criteria: RR >35, SpO₂ <90%, HR change >20%, BP change >20%, agitation, diaphoresis, accessory muscle use. If SBT passed, proceed to extubation. Daily SBT is superior to progressive SIMV weaning (Esteban 1995) — SIMV weaning is the slowest method and should be avoided as a primary weaning strategy.
4	Cuff leak test: deflate ETT cuff and listen for leak around tube with positive pressure breath. Absence of cuff leak (no audible leak) predicts post-extubation stridor, particularly in patients ventilated >36 hours. In at-risk patients (female sex, traumatic intubation, prolonged intubation), systemic steroids 12–24 hours before extubation (methylprednisolone 20 mg q4h × 4 doses) reduce post-extubation stridor and re-intubation (LANCET trial).
5	Post-extubation NIV/HFNC: In high-risk patients (age >65, cardiac/respiratory comorbidity, hypercapnic), preventive NIV immediately post-extubation reduces re-intubation rates (Ferrer 2006). HFNC is non-inferior to NIV in preventing re-intubation in high-risk patients (Hernandez 2016). However, in patients who have ALREADY developed post-extubation respiratory failure, NIV does NOT prevent re-intubation and may delay it dangerously — re-intubation must not be delayed once post-extubation failure is established.

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Shock — Classification & Pathophysiology

description Clinical Response

PHYSIOLOGY

1	Shock is defined as life-threatening, generalised circulatory failure resulting in cellular oxygen utilisation inadequate for metabolic demands. The four classes are: Distributive (septic, anaphylactic, neurogenic — vasodilation → ↓SVR → ↑CO initially); Hypovolaemic (haemorrhagic, dehydration — ↓preload → ↓CO); Cardiogenic (MI, cardiomyopathy — ↓pump function → ↓CO → ↑SVR); Obstructive (PE, tamponade, tension pneumothorax — mechanical obstruction to flow → ↓CO).
2	Haemodynamic fingerprinting is exam-critical: Distributive shock — ↓SVR, ↑CO, warm extremities, wide pulse pressure, low DBP. Cardiogenic shock — ↑SVR, ↓CO, cool extremities, S3 gallop, elevated JVP, pulmonary oedema. Hypovolaemic — ↑SVR, ↓CO, ↓PAWP. Obstructive (tamponade) — ↑SVR, ↓CO, ↑JVP, muffled heart sounds, pulsus paradoxus >10 mmHg, equalisation of diastolic pressures on right heart catheterisation.
3	ATLS Haemorrhagic Shock Classification: Class I (<750 mL, <15%): no change; Class II (750–1500 mL, 15–30%): HR↑, pulse pressure ↓, anxiety; Class III (1500–2000 mL, 30–40%): HR↑↑, BP↓, RR↑, confusion; Class IV (>2000 mL, >40%): HR↑↑, BP↓↓, lethargy, imminent death. Note: BP is the LAST parameter to fall — class III haemorrhage can have normal systolic BP. HR and pulse pressure are earlier indicators.
4	MAP = CO × SVR = (HR × SV) × SVR. Organ perfusion pressure = MAP − venous back-pressure. Target MAP ≥65 mmHg in septic shock (higher 80–85 in chronic hypertension — SEPSISPAM trial). MAP <65 mmHg for >30 minutes is associated with AKI, cardiac injury, and mortality. In haemorrhagic shock, permissive hypotension (MAP 50–65) until surgical haemostasis reduces coagulopathy and re-bleeding — do NOT target normal MAP in uncontrolled haemorrhage.
5	Fluid responsiveness: only ~50% of haemodynamically unstable ICU patients are fluid-responsive. Static markers (CVP, PAWP) are unreliable predictors. Dynamic markers — pulse pressure variation (PPV) and stroke volume variation (SVV) — are reliable in mechanically ventilated patients in sinus rhythm with VT ≥8 mL/kg and no spontaneous breathing efforts. PPV/SVV >13% predicts fluid responsiveness. Passive Leg Raise (PLR) test: reversible autotransfusion of ~300 mL — CO increase ≥10% by non-invasive CO monitoring confirms fluid responsiveness even in spontaneously breathing patients.

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Sepsis & Septic Shock — Surviving Sepsis 2021

description Clinical Response

GUIDELINE

1	Sepsis-3 Definition (Singer, JAMA 2016): Sepsis = life-threatening organ dysfunction caused by dysregulated host response to infection. Operationally defined as SOFA score ≥2 points above baseline. Septic shock = sepsis + vasopressor requirement to maintain MAP ≥65 + lactate >2 mmol/L despite adequate fluid resuscitation. SIRS criteria are no longer part of the definition — they lack specificity and have been replaced by organ dysfunction scoring.
2	qSOFA (quick SOFA) as a bedside screening tool: RR ≥22/min + altered mentation (GCS <15) + systolic BP ≤100 mmHg. Score 2–3 = high risk of poor outcome — warrants further assessment with full SOFA. qSOFA has higher specificity but lower sensitivity than SIRS for identifying sepsis. It is a screening tool only, not a diagnostic criterion for sepsis.
3	Surviving Sepsis Hour-1 Bundle (SSC 2018/2021): Within 1 hour — (1) Measure lactate (re-measure if initial lactate >2 mmol/L); (2) Obtain blood cultures BEFORE antibiotics; (3) Administer broad-spectrum antibiotics; (4) Begin 30 mL/kg crystalloid for hypotension or lactate ≥4; (5) Apply vasopressors if hypotension persists to target MAP ≥65 mmHg. Antibiotic delay beyond 1 hour increases mortality by 7% per hour in septic shock.
4	Fluid resuscitation: 30 mL/kg IV crystalloid within 3 hours in sepsis-induced hypoperfusion — but the FEAST and CLOVERS trials show excessive fluid causes harm. After initial resuscitation, reassess fluid responsiveness before each additional bolus. Balanced crystalloids (Lactated Ringer's, PlasmaLyte) are preferred over 0.9% normal saline — SMART trial showed NS associated with higher MAKE30 (major adverse kidney events) vs balanced crystalloids in critically ill patients.
5	Source control: achieve within 6–12 hours of diagnosis. Remove infected catheters, drain abscesses, debride necrotic tissue. Biliary sepsis requires biliary drainage; urological source requires decompression. Hydrocortisone in septic shock: ADRENAL trial (2018) — 200 mg/day infusion reduces time on vasopressors but not 90-day mortality in unselected patients. SSC 2021 recommends hydrocortisone for vasopressor-refractory septic shock (noradrenaline ≥0.25 mcg/kg/min after adequate fluid resuscitation for ≥4 hours).
6	Vitamin C + Hydrocortisone + Thiamine (HAT therapy): Marik protocol generated initial enthusiasm but the VITAMINS trial (2020), CITRIS-ALI, and VICTAS trials found no mortality benefit vs hydrocortisone alone. HAT therapy is NOT recommended by SSC 2021. Glucose control target: 144–180 mg/dL (8–10 mmol/L) — NICE-SUGAR trial demonstrated that tight control (81–108 mg/dL) increased mortality; moderate glycaemic control is the current standard.

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Vasopressors & Inotropes in the ICU

description Clinical Response

PHARMACOLOGY

1	Noradrenaline (norepinephrine) is the first-line vasopressor in septic shock (SSC 2021, strong recommendation). Predominantly α₁ agonist (vasoconstriction) with modest β₁ (positive inotropy). Dose: 0.01–3 mcg/kg/min. Increases MAP primarily through ↑SVR. Reflex bradycardia can occur. Should be given via central venous access (although short-term peripheral administration at low doses is increasingly practiced in resource-limited settings per ACEP guidance).
2	Vasopressin: V1 receptor-mediated vasoconstriction, independent of adrenoreceptors. Added to noradrenaline as a vasopressor-sparing strategy (VASST trial). Recommended at a fixed dose of 0.03 units/min — higher doses cause coronary, splanchnic, and digital ischaemia. Relative vasopressin deficiency occurs in septic shock. Particularly useful when noradrenaline requirements are high (>0.25 mcg/kg/min) or in patients with atrial fibrillation (avoids catecholamine-driven tachycardia).
3	Adrenaline (epinephrine): α + β agonist. Used as second-line vasopressor in septic shock, first-line in anaphylactic shock and cardiac arrest. Causes hyperglycaemia and hyperlactataemia (β₂-mediated glycogenolysis and aerobic lactate production) — can obscure lactate-guided resuscitation. Dopamine: at low doses (1–3 mcg/kg/min) — DA receptor, renal vasodilation (no longer recommended for "renal protection"); mid-dose (3–10 mcg/kg/min) — β₁, ↑CO; high-dose (>10 mcg/kg/min) — α₁, ↑SVR. SOAP II trial: dopamine vs noradrenaline — increased arrhythmia risk with dopamine; no mortality difference overall, but higher mortality in cardiogenic shock subgroup.
4	Dobutamine: predominantly β₁ (↑inotropy, ↑HR) with mild β₂ (vasodilation). First-line inotrope in cardiogenic shock with preserved MAP. Dose: 2.5–20 mcg/kg/min. Can cause hypotension (vasodilation) and tachyarrhythmias — often combined with noradrenaline in cardiogenic shock. Milrinone: PDE-III inhibitor — ↑cAMP → ↑inotropy + vasodilation (inodilator). Preferred when β-blocker therapy makes dobutamine less effective. Prolonged half-life (2–4 hours) makes dose titration slower — renally cleared, use with caution in AKI.
5	Levosimendan: calcium sensitiser + K-ATP channel opener. Improves inotropy without increasing myocardial O₂ consumption (unlike catecholamines). Active metabolite OR-1896 provides effects for up to 7–9 days after a 24-hour infusion. LIDO, SURVIVE trials: non-inferior or superior to dobutamine. Approved in India/Europe for acute decompensated heart failure. Causes vasodilation and hypotension — requires careful patient selection. Not FDA-approved in the USA.

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Fluid Resuscitation — Crystalloids vs Colloids

description Clinical Response

CLINICAL

1	Normal Saline (0.9% NaCl): Na 154 mmol/L, Cl 154 mmol/L, pH 5.5. Hyperchloraemic metabolic acidosis with large-volume infusion — excess chloride causes renal afferent arteriolar vasoconstriction, reducing GFR. SMART trial (Semler 2018): balanced crystalloids reduced MAKE30 events vs NS in critically ill patients. NS remains appropriate for specific situations: hypochloraemic metabolic alkalosis, head trauma (avoid hypotonic solutions), neurosurgical patients (osmolarity concern).
2	Hartmann's/Lactated Ringer's: Na 130, K 4, Ca 1.5, Cl 109, lactate 28 mmol/L. Slightly hypotonic (osmolarity 273 mOsm/L) — avoid as monotherapy in head injury or hyponatraemia. The lactate is metabolised hepatically to bicarbonate. PlasmaLyte 148 is the most physiologically balanced (pH 7.4, osmolarity 294 mOsm/L, acetate and gluconate as buffers instead of lactate) — preferred in liver disease where lactate metabolism is impaired.
3	Albumin: SAFE trial (2004) — albumin vs NS for ICU resuscitation: equivalent outcomes overall, but albumin was harmful in TBI (higher ICP) and beneficial in severe sepsis subgroup. ALBIOS trial (2014) — 20% albumin targeting serum albumin ≥30 g/L did not reduce 28-day mortality in sepsis (but reduced vasopressor days). Use albumin as the fluid of choice in spontaneous bacterial peritonitis (SBP) and hepatorenal syndrome — these are evidence-based specific indications where albumin is superior.
4	Hydroxyethyl Starch (HES) — CONTRAINDICATED in ICU: 6S trial (Perner 2012) and CHEST trial (Myburgh 2012) demonstrated HES causes AKI and increases need for renal replacement therapy in sepsis and ICU patients respectively. EMA suspended HES licence for critically ill patients in 2018. Gelatin solutions (Gelofusine): widely used but evidence limited; may also impair haemostasis and cause anaphylaxis. Dextrans cause platelet dysfunction and anaphylaxis — rarely used.
5	The Starling principle revision (revised Starling model): classic Starling forces assumed fluid freely moves between capillary and interstitium based on oncotic and hydrostatic pressure gradients. The glycocalyx layer — a proteoglycan meshwork lining the capillary endothelium — acts as the true oncotic barrier. Damage to the glycocalyx (sepsis, surgery, ischaemia-reperfusion) causes fluid shift regardless of plasma oncotic pressure. This explains why large crystalloid volumes cause oedema even when albumin levels are normal — preserving the glycocalyx (minimising hypervolaemia, using albumin) is the modern rationale for restrictive fluid therapy.

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Haemodynamic Monitoring — Invasive & Non-Invasive

description Clinical Response

MONITORING

1	Pulmonary Artery Catheter (PAC / Swan-Ganz): measures RAP (CVP), RV pressures, PA pressure, PAWP (wedge), mixed venous O₂ saturation (SvO₂), and thermodilution CO. Normal PAWP 6–12 mmHg — estimates left atrial pressure and LV preload. PAWP >18 mmHg suggests cardiogenic pulmonary oedema; PAWP ≤18 with P/F <300 suggests ARDS/non-cardiogenic oedema. PAC use has declined — PACMAN and ESCAPE trials showed no outcome benefit in unselected patients; PAC remains valuable in complex haemodynamics (pulmonary hypertension, mixed shock states, right heart failure).
2	Arterial line (radial artery preferred): continuous beat-to-beat BP, arterial waveform analysis. The arterial waveform provides pulse pressure variation (PPV) — area under the systolic waveform varies with respiratory cycle in mechanically ventilated patients; PPV >13% indicates fluid responsiveness. The dicrotic notch represents aortic valve closure (end of systole) — its position on the waveform reflects SVR; early dicrotic notch = low SVR (vasodilated); late notch = high SVR.
3	Transpulmonary thermodilution (PiCCO/LiDCO): allows measurement of CO, global end-diastolic volume (GEDV — preload marker superior to CVP), extravascular lung water (EVLW — quantifies pulmonary oedema), and continuous PPV/SVV. EVLW >10 mL/kg IBW indicates significant pulmonary oedema — useful for guiding de-resuscitation. PiCCO requires femoral artery catheter + central venous catheter — less invasive than PAC but still provides advanced haemodynamic data.
4	Point-of-Care Ultrasound (POCUS) in the ICU — RUSH protocol (Rapid Ultrasound for Shock and Hypotension): Pump (cardiac — LV/RV function, tamponade, wall motion); Tank (volume status — IVC collapsibility: IVC <2.1 cm with >50% collapse = low CVP ≈ fluid responsive; IVC plethoric = elevated CVP); Pipes (aorta — AAA; deep veins — DVT as PE source). Lung ultrasound: B-lines (≥3 per zone = interstitial syndrome/pulmonary oedema); absence of lung sliding = pneumothorax.
5	Near-infrared spectroscopy (NIRS/rSO₂): non-invasive regional O₂ saturation monitoring — applied to forehead (cerebral), thenar (peripheral). rSO₂ <50% or drop >20% from baseline signals inadequate regional DO₂. Capillary refill time (CRT): >2 seconds indicates peripheral hypoperfusion. The ANDROMEDA-SHOCK trial showed CRT-guided resuscitation was non-inferior to lactate-guided resuscitation in septic shock — CRT is a valid, universally available resuscitation endpoint. Skin mottling score (0–5) correlates with outcomes in septic shock.

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Acute Kidney Injury in the ICU

description Clinical Response

CRITICAL

1	KDIGO AKI Staging: Stage 1 — SCr ×1.5–1.9 from baseline OR increase ≥0.3 mg/dL within 48h OR UO <0.5 mL/kg/h for 6–12h. Stage 2 — SCr ×2–2.9 OR UO <0.5 mL/kg/h for ≥12h. Stage 3 — SCr ×3 OR ≥4 mg/dL OR RRT initiated OR UO <0.3 mL/kg/h for ≥24h or anuria ≥12h. KDIGO AKI is a revision of RIFLE (Risk, Injury, Failure, Loss, ESRD) and AKIN criteria — KDIGO is now the universal standard.
2	Causes in the ICU: Prerenal (most common — hypovolaemia, low CO, renal artery stenosis); Intrinsic renal (ATN from ischaemia or nephrotoxins — aminoglycosides, contrast, vancomycin, NSAIDs); Postrenal (obstruction — rare in ICU). FENa (fractional excretion of sodium) = (UCr × PNa)/(PCr × UNa) × 100. FENa <1% = prerenal (tubular sodium avidity); FENa >2% = ATN (tubular injury impairs sodium reabsorption). FENa is unreliable with diuretics — use FEUrea (<35% = prerenal) instead.
3	Contrast-Induced AKI (CI-AKI): defined as SCr rise ≥0.3 mg/dL or ≥50% within 48–72h of iodinated contrast. Risk factors: pre-existing CKD (eGFR <45), diabetes, hypovolaemia, heart failure, NSAIDs, large contrast volume. Prevention: IV hydration (NS or NaHCO₃) before and after contrast; use iso-osmolar/low-osmolar contrast; minimise contrast volume; hold nephrotoxins 24–48h. N-acetylcysteine: despite widespread use, meta-analyses show no consistent benefit — not routinely recommended.
4	Renal Replacement Therapy (RRT): indications — AEIOU: Acidosis refractory (pH <7.1); Electrolyte (K >6.5 refractory); Ingestion/toxic (methanol, ethylene glycol, lithium); Overload (refractory pulmonary oedema); Uraemia symptoms (encephalopathy, pericarditis, bleeding). AKIKI trial (2016): no benefit to early vs delayed RRT initiation in AKI; delaying RRT allows spontaneous recovery in ~49% — avoid premature initiation unless emergent indications exist.
5	CRRT vs intermittent haemodialysis (IHD): CRRT preferred in haemodynamically unstable patients (slower solute and fluid removal prevents hypotension); IHD preferred for rapid toxin removal and when anticoagulation is contraindicated for prolonged periods. CRRT dose: 20–25 mL/kg/h of effluent (RENAL and ATN trials — higher doses do not improve outcomes). Anticoagulation: regional citrate (chelates calcium in circuit, minimised systemic effect) is preferred; unfractionated heparin is alternative.

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Acid-Base Disorders — Stewart Approach

description Clinical Response

PHYSIOLOGY

1	Traditional Henderson-Hasselbalch approach: pH = pKa + log [HCO₃⁻]/[CO₂]. Primary disorders and compensatory responses — metabolic acidosis: ↓HCO₃⁻, respiratory compensation (↑RR) = Winter's formula: expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2. Metabolic alkalosis: ↑HCO₃⁻, respiratory compensation (hypoventilation) = expected PaCO₂ = (0.7 × HCO₃⁻) + 21. Respiratory acidosis: acute — HCO₃⁻ rises 1 per 10 mmHg CO₂; chronic — HCO₃⁻ rises 3.5 per 10 mmHg CO₂.
2	Anion Gap (AG) = Na − (Cl + HCO₃⁻). Normal: 8–12 mEq/L. Elevated AG metabolic acidosis mnemonic — MUDPILES: Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol/Paracetamol, Isoniazid/Iron, Lactic acidosis, Ethylene glycol, Salicylates. Correct AG for albumin: add 2.5 mEq/L for each 1 g/dL fall in albumin below 4 g/dL (critical in ICU where hypoalbuminaemia is common and can mask elevated AG). Normal AG metabolic acidosis — HARDUPS: Hyperalimentation, Addison's, RTA, Diarrhoea, Ureteral diversion, Pancreatic fistula, Saline infusion.
3	Delta-Delta ratio (ΔAG/ΔHCO₃⁻): in elevated AG metabolic acidosis, determines if additional metabolic process is present. ΔAG = actual AG − 12; ΔHCO₃⁻ = 24 − actual HCO₃⁻. Ratio <0.4 = hyperchloraemic (non-gap) component present; 0.4–0.8 = mixed gap and non-gap; 0.8–2 = pure elevated AG acidosis; >2 = concomitant metabolic alkalosis. This is a frequently examined calculation in DNB/MD exams.
4	Stewart (physicochemical) approach: only three independent variables determine pH — PaCO₂ (respiratory), strong ion difference (SID = Na + K + Ca + Mg − Cl − lactate) (metabolic; normal SID ≈ 40 mEq/L), and total weak acid concentration (ATOT = albumin + phosphate). ↑SID = alkalosis; ↓SID = acidosis. Normal saline lowers SID (adds equal Na and Cl) → acidosis even with normal AG. Hypoalbuminaemia raises pH (alkalosis) because albumin is a weak acid — explains why ICU patients often have complex, mixed disorders masked by traditional analysis.
5	Lactic acidosis: Type A (tissue hypoxia — shock, cardiac arrest, CO poisoning, severe anaemia) vs Type B (no hypoperfusion — metformin, thiamine deficiency, malignancy, liver failure, nucleoside analogues). Lactate >2 mmol/L = hyperlactataemia; >4 mmol/L = significant hyperlactataemia. In sepsis, lactate >2 mmol/L despite MAP ≥65 = septic shock. Serial lactate measurement every 2 hours — clearance ≥10% at 2h is an acceptable resuscitation endpoint. Failure to clear lactate is a strong predictor of mortality.

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Sedation, Analgesia & Delirium in ICU (PADIS Guidelines)

description Clinical Response

PHARMACOLOGY

1	PADIS Guidelines 2018 (Pain, Agitation/Sedation, Delirium, Immobility, Sleep disruption): the paradigm shift — analgesia FIRST, then sedation (analgesia-based sedation reduces ventilator days, ICU stay, and opioid use). Target sedation: RASS (Richmond Agitation-Sedation Scale) −1 to 0 (light sedation) for most ICU patients. Daily sedation interruption (DSI) or targeting light sedation reduces ventilator days (Kress 2000, ABC trial) — remains standard practice.
2	Propofol: GABA agonist, rapid onset/offset, antiemetic, anticonvulsant. Preferred for short-term ICU sedation. Propofol Infusion Syndrome (PRIS): metabolic acidosis, rhabdomyolysis, cardiac failure, renal failure, lipaemic plasma — occurs with doses >4 mg/kg/h for >48h, particularly in children and patients receiving catecholamines/steroids. Monitor CK, triglycerides, and lactate. Limit propofol to ≤4 mg/kg/h; maximum 80 mg/kg/day.
3	Dexmedetomidine: α₂ agonist (central — reduces noradrenaline release → sedation, anxiolysis, analgesia). Unique property: patients are sedated but arousable — preserves natural sleep architecture, maintains respiratory drive (safe to use with spontaneous breathing). MENDS2 and SPICE III trials: dexmedetomidine reduces delirium compared to propofol/midazolam. Causes bradycardia and hypotension — use cautiously with β-blockers or in cardiogenic shock. Increasingly preferred for light sedation in ICU.
4	ICU Delirium: defined by CAM-ICU (Confusion Assessment Method for ICU) — requires (1) acute onset/fluctuating course + (2) inattention + (3) disorganised thinking OR (4) altered consciousness. Delirium affects 60–80% of mechanically ventilated patients. Hypoactive delirium (quiet, withdrawn) is more common and more often missed than hyperactive delirium. Risk factors: pre-existing cognitive impairment, age, prior alcohol/substance use, severity of illness, immobility, sleep deprivation, benzodiazepines.
5	Prevention: ABCDEF bundle — Analgesia-first; Both awakening and breathing trials (SAT + SBT); Choice of sedation; Delirium monitoring/management; Early mobility and exercise; Family engagement. Haloperidol: does NOT reduce delirium duration (MIND, HOPE-ICU, REDUCE trials) — not recommended prophylactically. Antipsychotics may shorten delirium episodes in hyperactive delirium. Benzodiazepines should be avoided in ICU sedation wherever possible — they are independent risk factors for delirium.

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Coagulation Disorders & Transfusion in the ICU

description Clinical Response

CRITICAL

1	Disseminated Intravascular Coagulation (DIC): simultaneous pathological activation of coagulation AND fibrinolysis. ISTH DIC Score: platelets, PT, fibrinogen, D-dimer — score ≥5 = overt DIC. Causes: sepsis (most common in ICU), trauma, obstetric catastrophe (abruption, AFE), malignancy, transfusion reactions, snake envenomation. Treatment is of the underlying cause; blood products are given for bleeding or procedural coverage, not to correct laboratory values alone.
2	Transfusion thresholds in ICU: Restrictive strategy (Hb 7 g/dL) is equivalent or superior to liberal (Hb 10 g/dL) in most ICU patients — TRICC trial. Exceptions where higher thresholds are used: active ACS (Hb <8–10), subarachnoid haemorrhage (Hb <8–9). Transfusion-Related Acute Lung Injury (TRALI): non-cardiogenic pulmonary oedema within 6 hours of transfusion — donor antibodies (anti-HLA, anti-neutrophil) activate recipient neutrophils in lungs. Leading cause of transfusion-related mortality. Treatment: supportive (may require mechanical ventilation).
3	Massive Haemorrhage Protocol (MHP): defined as transfusion of ≥10 units pRBC in 24h, or ≥4 units in 1h. Damage control resuscitation: balanced blood product ratio (pRBC : FFP : platelets = 1:1:1 — PROPPR trial); permissive hypotension (SBP 80–90 until surgical haemostasis); early tranexamic acid (CRASH-2: within 3 hours of injury, reduces mortality in haemorrhagic trauma — 1g IV over 10 min, then 1g over 8h); avoid hypothermia, acidosis, hypocalcaemia (lethal triad).
4	Viscoelastic haemostatic assays (VHA): ROTEM (Rotational Thromboelastometry) and TEG (Thromboelastography) provide real-time analysis of clot formation, strength, and lysis — allowing targeted, goal-directed transfusion rather than empirical product replacement. ITACTIC trial: VHA-guided transfusion did not reduce mortality vs conventional coagulation-guided transfusion in trauma — but reduced exposure to FFP and platelets. VHA is most valuable in cardiac surgery, liver transplantation, and massive haemorrhage.
5	Heparin-Induced Thrombocytopenia (HIT): immune-mediated platelet activation by anti-PF4/heparin antibodies. Platelet fall 50% or to <100 × 10⁹/L, days 5–14 of heparin exposure (or immediate re-exposure). Paradoxical thrombosis risk (not bleeding) despite thrombocytopenia. 4T score assesses pre-test probability. Management: stop all heparin immediately (including flushes, heparin-coated catheters); initiate non-heparin anticoagulant — argatroban (hepatic metabolism, preferred in renal failure), fondaparinux, bivalirudin. Warfarin contraindicated acutely (risk of venous gangrene via protein C depletion).

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Anesthesia

Weaning from Mechanical Ventilation

Shock — Classification & Pathophysiology

Sepsis & Septic Shock — Surviving Sepsis 2021

Vasopressors & Inotropes in the ICU

Fluid Resuscitation — Crystalloids vs Colloids

Haemodynamic Monitoring — Invasive & Non-Invasive

Acute Kidney Injury in the ICU

Acid-Base Disorders — Stewart Approach

Sedation, Analgesia & Delirium in ICU (PADIS Guidelines)

Coagulation Disorders & Transfusion in the ICU

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