class: center, middle name: countdown-slide <style> #progress-ring { transition: stroke-dashoffset 1s linear, stroke 0.3s ease; } </style> # Quiet please in... <div style="position: relative; width: 500px; height: 500px; margin: 0 auto;"> <svg width="500" height="500" style="transform: rotate(-90deg);"> <circle cx="250" cy="250" r="230" stroke="#e0e0e0" stroke-width="20" fill="none" /> <circle id="progress-ring" cx="250" cy="250" r="230" stroke="#2c7be5" stroke-width="20" fill="none" stroke-linecap="round" stroke-dasharray="1445.9" stroke-dashoffset="0" /> </svg> <div id="countdown" style="position: absolute; top: 50%; left: 50%; transform: translate(-50%, -50%); font-size: 10em; font-weight: bold; font-family: sans-serif;"> </div> </div> <script> (function() { var el = document.getElementById("countdown"); var ring = document.getElementById("progress-ring"); var timer = null; var radius = 230; var circumference = 2 * Math.PI * radius; // β 1445.9 function setProgress(fraction) { var offset = circumference * (1 - fraction); ring.style.strokeDashoffset = offset; } function startCountdown() { // Clear any existing timer so re-entering the slide restarts cleanly if (timer) { clearInterval(timer); timer = null; } var total = 10; var count = total; el.innerHTML = count; ring.style.stroke = "#2c7be5"; setProgress(count / total); timer = setInterval(function() { count--; el.innerHTML = count; setProgress(count / total); if (count <= 3) { ring.style.stroke = "#e63946"; } if (count <= 0) { clearInterval(timer); timer = null; el.innerHTML = "π€«"; ring.style.stroke = "#2ecc71"; } }, 1000); } slideshow.on('afterShowSlide', function (slide) { if (slide.properties.name === "countdown-slide") { startCountdown(); } }); })(); </script> --- class: intro-slide <div class="intro-left"> <div class="qr-item"> <p class="qr-caption">To log attendance:</p> <img src="images/qr_attendance.png" alt="Attendance QR code" /> </div> <!-- <div class="qr-item"> --> <!-- <p class="qr-caption">To log into Wooclap:</p> --> <!-- <img src="images/qr_wooclap.png" alt="Wooclap QR code" /> --> <!-- </div> --> </div> <div class="intro-right" id="vanta-bg"> <div class="intro-right-content"> <h1>AKI & IV Fluid Therapy</h1> <h2>Y4 MBChB Tutorial 2026-7 | Rob Hunter</h2> <div class="intro-spacer"></div> .callout-question[ **Two questions for you:** - what % of hospital patients have AKI? - what % of all doctors are nephrologists? ] </div> </div> <script> (function initVantaIntro(attempts) { attempts = attempts || 0; var target = document.getElementById("vanta-bg"); if (typeof VANTA === "undefined" || !target || target.offsetWidth === 0) { if (attempts < 20) { setTimeout(function () { initVantaIntro(attempts + 1); }, 150); } return; } VANTA.BIRDS({ el: target, mouseControls: true, touchControls: true, gyroControls: false, minHeight: 200.00, minWidth: 200.00, scale: 1.00, scaleMobile: 1.00, backgroundColor: 0xffffff, color1: 0x3c00ff, color2: 0xffa400, birdSize: 1.20, speedLimit: 3.00, quantity: 3.00 }); })(); </script> ??? --- # Why should we care? ### AKI: - common: 10 - 20% of all hospital admissions - serious: 10 - 20% inpatient mortality <br> ### IV Fluids: - prescribing often delegated to junior staff - preventable harm in ~20% of patients on IV fluids <br> ??? Prompt: Why do you think fluid prescribing is often poorly done, despite being so common? (Junior doctors, time pressure, lack of formal teaching, assumption it's simple.) --- class: image-left .left-panel.navy[ #### Playbooks: - AKI - IV fluids (assessment) - IV fluids (prescribing) ] # Learning outcomes #### Acute Kidney Injury - Define AKI using KDIGO criteria - Classify causes: **pre-renal, intrinsic, post-renal** - Structure an assessment and outline management principles <br> #### IV Fluid Therapy - Apply the **5 Rs framework** to fluid prescribing decisions - Choose an appropriate **fluid type, volume & rate** - Recognise when fluids may be **harmful** <br> #### Cases - Apply all of the above to **4 realistic clinical scenarios**, using real fluid charts ??? Ask students what they hope to get out of today before revealing objectives. --- class: section, middle # Part 1 ## Acute Kidney Injury --- # AKI definition -- AKI is diagnosed if **any one** of the following is present (KDIGO/NICE): - Serum creatinine rise of **β₯26 ΞΌmol/L within 48 hours** - Serum creatinine rise to **β₯1.5Γ baseline** within 7 days - Urine output **<0.5 mL/kg/hour for β₯6 hours** .callout.callout-bottom[ **Key concept.** AKI is a **syndrome**, not a diagnosis. It describes a *spectrum* of kidney injury β not just kidney failure β and always demands a search for an underlying cause. ] -- <br> #### Staging .compact-table[ | Stage | Creatinine | Urine output | |:--|:--|:--| | 1 | 1.5β1.9Γ baseline, or β₯26 ΞΌmol/L rise | <0.5 mL/kg/h for 6β12h | | 2 | 2.0β2.9Γ baseline | <0.5 mL/kg/h for β₯12h | | 3 | β₯3.0Γ baseline, or β₯354 ΞΌmol/L, or KRT started | <0.3 mL/kg/h β₯24h or anuria β₯12h | ] ??? Prompt: Why might urine output be a more sensitive early sign than creatinine? Stage using **whichever criterion gives the higher (worse) stage**. Higher AKI stage = higher mortality risk and higher likelihood of needing renal replacement therapy. Even *minor* creatinine rises are associated with increased mortality. Baseline = lowest value in last 7 days, or lowest/mean value from 7 daysβ3 months if no recent value available. --- # AKI causes --  --- # AKI causes  --- # AKI causes .pull-left[ ### Pre-renal (~80%) Reduced *perfusion* β no structural damage (yet): - Hypovolaemia (bleeding, D&V, poor intake) - Sepsis / hypotension - Heart failure, cirrhosis (reduced effective circulating volume) - Drugs: NSAIDs, ACEi/ARB, diuretics ] .pull-right[ ### Intrinsic (~10β20%) *Structural damage* to the kidney: - Acute tubular injury (ATI: most common β often prolonged pre-renal insult) - Glomerulonephritis / vasculitis - Interstitial nephritis (drugs, infection) - Rhabdomyolysis, myeloma <br> ### Post-renal (~5β10%) Urinary tract *obstruction*: - Prostatic hyperplasia, stones, malignancy ] ??? Prompts: - What determines whether pre-renal AKI progresses to ATN? (severity & duration) - Can you have pre-renal AKI and be fluid overloaded at the same time? <br> Pre-renal AKI is a **functional, reversible** response to reduced perfusion β **no structural damage has yet occurred**. - Kidneys try to preserve GFR via **RAAS activation** and **ADH release** - Sodium and water are avidly retained > low urine sodium (<20 mmol/L) - **Reversible** with prompt correction of perfusion β but prolonged or severe hypoperfusion leads to **acute tubular necrosis** (no longer reversible on restoring perfusion alone) **Common pitfall.** Don't assume "pre-renal" always means "just give fluids." In cardiac failure or cirrhosis, effective circulating volume is *low* despite **total body fluid overload** β more fluid can cause harm. --- # AKI: history - **Fluid intake and losses**: vomiting, diarrhoea, bleeding, poor oral intake, fever, stoma output, polyuria - **Comorbidities**: CKD, heart failure, liver disease, diabetes - **Medications**: - NSAIDs, ACE inhibitors/ARBs, diuretics, aminoglycosides - SGLT2 inhibitors (?) β increasingly recognised as a "sick day" risk - metformin, opioids... - **Urinary symptoms**: LUTS suggesting obstruction - **Systemic features**: rash, joint pain, haemoptysis ??? Note the addition of SGLT2 inhibitors reflects recent MHRA safety updates (2020 onwards) β flag this as an evolving area students should know for AKT. --- # AKI: examination .pull-left[ ### Volume status - Pulse, BP (including postural), JVP - Capillary refill, mucous membranes, skin turgor - Peripheral/pulmonary oedema - Urine output (catheter if needed) ] .pull-right[ ### Look for a cause - Peripheral pulses - Abdominal/pelvic mass, palpable bladder - Rash, joint swelling, red eyes, foot drop... - Signs of infection ] <br> .callout[ **Tachycardia often precedes hypotension** as a sign of hypovolaemia β compensatory vasoconstriction can maintain BP until significant volume loss has occurred. Don't be falsely reassured by a normal BP. ] .callout-warn[ Older/frail patients may not mount tachycardia (e.g., on beta-blockers) β postural BP drop may be the only clue. ] --- # AKI: investigations #### Core set - **U&Es** (creatinine trend, potassium, sodium, bicarbonate) β compare to baseline - FBC, CRP, LFTs, calcium - **Urinalysis**: blood + protein = intrinsic - ECG if hyperkalaemia <br> #### Consider - Renal tract ultrasound β **only if no clear cause**, or obstruction/pyonephrosis suspected - Blood film, CK (rhabdomyolysis), serum/urine electrophoresis (myeloma, if >40y) - Immunology (ANCA, ANA, complement) if intrinsic renal disease suspected ??? Reinforce that USS is not routine β NICE NG148 explicitly says do not offer it routinely once a cause is identified. Only escalate if no clear cause, or obstruction/pyonephrosis suspected (urgent, within 6h if pyonephrosis). --- # AKI: management 1. Treat the **underlying cause** (e.g. infection, obstruction) 2. Optimise **fluid status** & monitor response 3. Review **medications** - stop/withhold nephrotoxins and drugs impairing renal autoregulation - stor/dose-adjust renally cleared drugs 4. Treat **complications**: hyperkalaemia, acidosis, fluid overload, uraemia 5. **Refer** to renal if: suspected intrinsic cause or heading towards KRT <br> .callout-warn[ **"Sick day rules"**: during acute illness with poor intake/D&V, temporarily stop ACEi/ARB, NSAIDs, diuretics, SGLT2 inhibitors, and metformin. ] ??? This is a heavily tested AKT concept. Ask students to try to name the "sick day" drug list from memory before revealing it (Socratic questioning / think-pair-share 30 seconds). --- class: image-left .left-panel.amber[ # TL;DR - pre-renal - intrinsic - post-renal ] # Recap: AKI on one slide - **Definition**: creatinine rise or oliguria <br> - **Causes**: pre-renal (80%) > intrinsic > post-renal β often multifactorial <br> - **Pre-renal AKI**: functional, reversible β but can progress to ATI if hypoperfusion persists <br> - **Assessment**: volume status + look for a cause <br> - **Management**: treat cause, optimise fluids, review drugs, treat complications, know when to refer ??? --- class: section, middle # Part 2 ## IV Fluid Therapy ---  ??? Thomas Latta (1832) --- # Types of fluid  --- class: image-left .left-panel.navy[ ] # Body fluid compartments  --- class: image-left .left-panel.navy.align-bottom[ <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> <br> For every 1L infused, intravascular volume will receive: - < 83 ml for 5% glucose - < 250 ml for 0.9% NaCl ] # Body fluid compartments  ??? Only **~25% of infused isotonic crystalloid stays intravascular** β the rest distributes into the interstitium. Large-volume crystalloid resuscitation can cause interstitial oedema even while correctly expanding circulating volume. --- # Before you prescribe: 4Qs & 5Rs .callout[ 1. **Does this patient need IV fluid at all?** 2. What **type** of fluid? 3. **How much?** & **how fast?** 4. How will I **monitor** the response β for both efficacy and safety? ] <br> | R | Meaning | |:--|:--| | **R**esuscitation | Correcting haemodynamic compromise | | **R**outine maintenance | Meeting daily needs when NBM/unsafe swallow | | **R**eplacement | Correcting ongoing abnormal losses or existing deficits | | **R**edistribution | Complex fluid shifts (oedema + hypovolaemia, sepsis, refeeding) | | **R**eassessment | Did it work? Is it still needed? | ??? IV fluid is a prescription β it carries the **same weight and risk** as any drug prescription. 5Rs are **not mutually exclusive**. A patient may need resuscitation, *then* maintenance, *plus* ongoing replacement of stoma losses β three separate prescribing decisions. ---  --- # Volume resuscitation - Isotonic crystalloid, NaβΊ **130β154 mmol/L** - **500 mL bolus over <15 minutes** - **Reassess** (pulse, BP, cap refill, urine output, NEWS) after every bolus - Repeat 250β500 mL boluses as needed <br> .callout-warn[ If **>2000 mL** given without haemodynamic improvement β **seek expert help**. This is beyond independent FY1 management. ] -- <br> .callout[ Balanced crystalloids generally *preferred* over 0.9% saline for resuscitation. Evidence is conflicting (SMART/SALT-ED *vs* BASICS/PLUS). Exceptions where 0.9% NaCl preferred: DKA; profuse vomiting; traumatic brain injury. ] ??? Emphasise the reassessment loop β this is not "give fluid and walk away." Passive leg raise can be introduced here as a bedside test of fluid responsiveness (rising BP = responsive; worsening breathlessness = overloaded). Prompt: why is the 2L safety rule built in? --- # Maintenance fluids Daily requirements for a **haemodynamically stable, euvolaemic** patient unable to take fluids enterally: | Component | Amount | |:--|:--| | Water | 25β30 mL/kg/day (20β25 in elderly/frail/renal/cardiac) | | Sodium, potassium, chloride | ~1 mmol/kg/day each | | Glucose | 50β100 g/day (prevents starvation ketosis only) | -- <br> .callout[ Standard UK regimen: **0.18% NaCl in 4% glucose**, with potassium as a **pre-mixed** bag (20 or 40 mmol/L) β round to nearest available strength. ] .callout-warn[ Prescribing **>2.5 L/day** of this hypotonic fluid increases the risk of **hyponatraemia**, especially post-operatively (non-osmotic ADH release). ] ??? Work a quick worked example on the board: 70kg patient β ~1750β2100mL water, ~70mmol each electrolyte, 50-100g glucose. This maps directly onto Case 2. --- # Replacement fluids - **Add to or subtract from** the maintenance prescription based on measured or estimated ongoing losses .compact-table[ | Loss Type | Na<sup>+</sup> | K<sup>+</sup> | Cl<sup>-</sup> | HCO<sub>3</sub><sup>-</sup> | Key Points | | :--- | :---: | :---: | :---: | :---: | :--- | | **Gastric / Vomit** | 20β60 | 10β20 | 140 | 0 | *chloride loss & H<sup>+</sup> > alkalosis* | | **Bile** | 140 | 5 | 90β110 | 30 | | | **Pancreatic** | 130β140 | 5 | 50β110 | 90β115 | *alkali loss > acidosis* | | **Small Bowel / Ileostomy** | 100β140 | 5 | 70β125 | 0-30 | | | **Diarrhoea** | 30β140 | 30β70 | - | 20β80 | *K-bicarbonate loss > hypoK acidosis* | ] -- <br> .callout-warn[ **IV potassium safety rules** (general ward): - Maximum concentration **40 mmol/L** - Maximum rate **10 mmol/hour** - Never give as a bolus; obtain ECG first if KβΊ <2.5 or >5.5 mmol/L ] ??? This slide directly sets up Case 4 (ileostomy patient). Ask students what electrolytes they'd expect to be lost in high stoma output (sodium, potassium, bicarbonate). --- # Monitoring patients on IV fluids - **Daily**: clinical fluid status, U&Es (inc. TCO<sub>2</sub>), fluid balance chart review - **Twice weekly**: body weight (1 kg change β 1 L fluid) - **Stop fluids** as soon as oral/enteral intake is adequate <br> .callout-question[ **Thinkβpairβshare (2 min)**: why might a fluid balance chart *underestimate* a patient's true fluid balance? Discuss with your neighbour, then feed back. ] <br> .callout-warn[ IV fluids can cause harm by causing: - **overload** in cardiac failure, cirrhosis, renal failure... - **hypoNa** with excessive hypotonic maintenance (esp. post-op) - **acidosis** with excessive 0.% NaCl o] ??? Answer: insensible losses (breathing, sweating, ~0.5β1 mL/kg/hr) are not usually charted. This is a nice subtle point for feedback. --- class: image-left .left-panel.amber[ # TL;DR - resuscitation - maintenance - replacement ] # Recap: IV fluids on one slide - Ask 4 questions before prescribing: need? type? volume/rate? monitoring? <br> - Use the **5 Rs**: Resuscitation, Routine maintenance, Replacement, Redistribution, Reassessment <br> - Prefer **balanced crystalloids** for resuscitation in most situations; know the exceptions <br> - Maintenance requirements = 'all the 1s' <br> - Fluid is a prescription like any other β review and stop it daily .callout-question.callout-bottom[ After a short break, get your pens out ready to prescribe fluids for our four cases! ] ??? Hand out fluid charts now if not already distributed. Explain the case format: each case has a "presentation" slide, then group discussion, then an "investigations" slide, then further group discussion and debrief. --- class: section, middle # Part 3 ## Cases ??? .callout-question.callout-bottom[ Work in groups. For each case, decide: 1) What extra information do you want? 2) What is your immediate management? 3) What fluid (if any) will you prescribe? ] ??? Read this slide aloud. Explain groups will have ~10-12 minutes per case: ~3 min after presentation slide, ~5 min after investigations slide, ~3-4 min debrief. Circulate during group work. --- .pull-left[  ] .pull-right[  .callout-question[ **For all cases:** 1) what extra information would you like? 2) if AKI then pre-renal, intrinsic or post? 3) what fluid would you prescribe? 4) other management? ] ] --- class: image-left .left-panel.top[  ] # 81 yo man with diarrhoea - 3 days of **diarrhoea** and poor oral intake, fever, productive cough - **PMH**: hypertension, T2DM, peripheral vascular disease - **O/E**: BP 92/56, pulse 108, dry mucous membranes, right basal crackles -- - **Ramipril** 10mg OD | **Bendroflumethiazide** 2.5mg OD | **Metformin** 1g BD - Ibuprofen (over-the-counter) -- <br> .compact-table[ | Test | Result | Reference Range | |:--|--:|:--| | Urea | **18.2** | 2.5β7.8 mmol/L | | Creatinine | **210** (baseline 120) | 60β110 ΞΌmol/L | | Sodium | 138 | 133β145 mmol/L | | Potassium | **5.7** | 3.6β5.5 mmol/L | | TCOβ (bicarbonate) | **17** | 22β30 mmol/L | | Hb | 138 | 130β170 g/L | | WBC | **14.2** | 4.0β11.0 Γ10βΉ/L | ] ??? Prompts: - what extra information do you want? (baseline SCr, u/o, NEWS, lactate, CXR...) - pre-renal, intrinsic or post-renal? - how would you manage him? (cultures, meds, fluids...) --- class: image-left .left-panel.top[  ]  --- class: image-left .left-panel.top[  ] # 76 yo woman with stroke - Large ischaemic stroke; **unsafe swallow** on SALT assessment - Nil by mouth pending further review - No prior regular medications; started on **aspirin and clopidogrel** - **Haemodynamically stable and euvolaemic** on examination - Estimated body weight **60 kg** -- <br> .compact-table[ | Test | Result | Reference Range | |:--|--:|:--| | Urea | 5.1 | 2.5β7.8 mmol/L | | Creatinine | 68 | 45β90 ΞΌmol/L | | Sodium | 140 | 133β145 mmol/L | | Potassium | 4.0 | 3.6β5.5 mmol/L | | TCOβ (bicarbonate) | 25 | 22β30 mmol/L | | Glucose | 5.8 | 4.0β7.8 mmol/L | ] ??? Prompts: - what extra information do you want? (could she have NG feeding?) - what fluids will you prescribe? --- class: image-left .left-panel.top[  ]  --- class: image-left .left-panel.top[  ] # 84 yo man with breathlessness - **1 week** of progressive breathlessness, **3 kg weight gain** - **PMH**: HFrEF, CKD, atrial fibrillation - **Medications**: candesartan, dapagliflozin, bisoprolol, bumetanide - **O/E**: BP 158/88, raised JVP, bibasal crackles, pitting oedema to knees <br> - A&E have already started IV **resuscitation fluids** for AKI -- <br> .compact-table[ | Test | Result | Reference Range | |:--|--:|:--| | Urea | **14.5** | 2.5β7.8 mmol/L | | Creatinine | **220** (baseline 140) | 60β110 ΞΌmol/L | | Sodium | **131** | 133β145 mmol/L | | Potassium | 5.1 | 3.6β5.5 mmol/L | | TCOβ (bicarbonate) | 24 | 22β30 mmol/L | ] ??? Prompt: - what extra information do you want? (recent diuretic compliance, weight trend, dapagliflozin as relevant sick-day drug) - what fluid would you prescribe? - how would you manage him? - pre-renal, intrinsic or post-renal? - how can he have an AKI when he is overloaded? --- class: image-left .left-panel.top[  ] # 58 yo woman, weak & dizzy - Recovering from emergency operation for diverticular perforation - New ileostomy - In pain, poor oral intake - **O/E**: BP 96/60, HR 104, dry mucous membranes - Pre-op weight 66 kg; weight now 62 kg -- <br> .compact-table[ | Test | Result | Reference Range | |:--|--:|:--| | Urea | **12.8** | 2.5β7.8 mmol/L | | Creatinine | **160** (baseline 90) | 45β90 ΞΌmol/L | | Sodium | **129** | 135β145 mmol/L | | Potassium | **3.1** | 3.6β5.5 mmol/L | | TCOβ (bicarbonate) | 27 | 22β30 mmol/L | ] ??? Prompts: - what extra information do you want? (stoma output volume over 24h, colour/consistency, full U&Es...) - what fluid would you prescribe? - what other management? (anti-motility agents e.g. loperamide) --- class: image-left .left-panel.top[  ]  --- class: section, middle # Part 4 ## Close --- # Reflection .pull-left[ ### Reflect - The **most important thing** I learned today was... - One thing I am **still unclear on** is... ] .pull-right[ ### Commit - One concrete thing I will **do differently** next time I'm involved in a patient's fluid management (as a student or FY1) ] ??? --- class: image-left .left-panel.amber[ # TL;DR - pre-renal - intrinsic - post-renal ] # Take-home points 1. AKI is a **syndrome**: always ask *why* and think pre-renal / intrinsic / post- 2. Pre-renal AKI is reversible β but can progress to **ATI** if hypoperfusion persists 3. Not all patients with AKI need more fluid 4. Prescribe IV fluid for **resuscitation**, **maintenance** or **replacement** 5. **Balanced crystalloids** are generally preferred for resusication (with exceptions) .callout-ref.callout-bottom[ See playbooks on: - AKI - IV fluids (assessment) - IV fluids (prescribing) ] --- class: center, middle  --- class: section, middle # Part 5 ## Supplemental slides --- # Crystalloids | Fluid | NaβΊ | KβΊ | Clβ» | Notes | |:--|--:|--:|--:|:--| | 0.9% NaCl | 154 | 0 | 154 | High chloride β risk of hyperchloraemic acidosis with large volumes | | Hartmann's | 131 | 5 | 111 | "Balanced" β lactate buffers to bicarbonate | | Plasma-Lyte 148 | 140 | 5 | 98 | "Balanced" β acetate/gluconate buffers | | 5% glucose | 0 | 0 | 0 | Distributes as free water β **not** for resuscitation | | 0.18% NaCl/4% glucose | 31 | 0 | 31 | Standard UK maintenance fluid (+ KCl) | <br> .callout[ Balanced crystalloids generally *preferred* over 0.9% saline for resuscitation. Evidence is conflicting (SMART/SALT-ED *vs* BASICS/PLUS). ] .callout-warn[ Exceptions where 0.9% NaCl preferred: DKA; profuse vomiting; traumatic brain injury. ] ??? Use this as a chance for critical appraisal discussion β guidelines (NICE CG174) have not yet fully caught up with BaSICS/PLUS. Flag this evidence- practice lag explicitly, as noted in the recent-updates summary β good AKT exam awareness point without over-simplifying "balanced is always better." **Never** add potassium chloride concentrate directly to a fluid bag at the bedside β this is a **Never Event** and can cause fatal cardiac arrest. Use pre-mixed bags only. --- # Colloids β mostly avoid .pull-left[ ### Use - **Red blood cells**: fluid of choice for active haemorrhage - Human albumin 4β5%: specific specialist indications only (e.g. SBP in cirrhosis) ] .pull-right[ ### Avoid - **Hydroxyethyl starch (HES)**: nephrotoxic β increases AKI and mortality. MHRA/EMA advise against use in **all** hospital inpatients - **Gelatins**: no proven benefit over crystalloid; anaphylaxis risk ] .callout-warn[ For FY1-level practice: use crystalloids for resuscitation and maintenance. Do not prescribe HES or gelatin. Albumin is a specialist decision. ] ??? This is a strong, easily testable "never do this" rule β good for AKT.