Access, modality and timing — three decisions made before a single litre of effluent is produced
Based on Koyner, Handbook of Critical Care Nephrology (2021) · NTUH Yunlin Branch
Learning objectives
Koyner Ch 29, 31–32, 56 · Ronco Ch 144, 163, 165–167, 179 · KDIGO AKI 2012
Every dose you fail to deliver, every filter you lose and half the infections you cause were decided at the moment the catheter went in.
“The access is the mother of dialysis.”
Negative arterial pressure without collapsing, 24 h a day for CRRT, in a patient who is coagulopathic, oedematous, proned and moved for imaging. Nothing about the prescription matters if the blood pump cannot be fed.
Koyner Ch 29 · KDIGO AKI 2012 Section 5 · Al Rifai A et al. Hemodial Int 2018;22:50 (AVF/AVG for CRRT)
| Site | Rank | Why | Catheter dysfunction |
|---|---|---|---|
| Right internal jugular | 1st | Shortest, straightest path to the cavoatrial junction; compressible; lowest recirculation | 6.6% |
| Femoral | 2nd | Fastest in an arrest or a coagulopathic patient; no pneumothorax risk; costs mobility | 10.3% |
| Left internal jugular | 3rd | Two near-right-angle turns before the SVC — kinking, tip malposition, worse flow | 19.5% |
| Subclavian | Last | Central vein stenosis destroys future fistula territory; not compressible if it bleeds | — |
750 ICU patients needing acute KRT randomised to femoral vs jugular: catheter colonisation 40.8 vs 35.7 per 1000 catheter-days (HR 0.85, 95% CI 0.62–1.16) with no difference in catheter-related bloodstream infection. Femoral was worse only in the highest BMI tertile (>28.4). Femoral access is a legitimate choice, not a compromise.
Parienti JJ et al. JAMA. 2008;299:2413–2422 · Parienti JJ et al. Crit Care Med. 2010;38:1118–1125 (dysfunction rates, n=736) · KDIGO 2012 · Koyner Ch 29
| Insertion site | Catheter length | Target tip |
|---|---|---|
| Right internal jugular | 15–20 cm | Right atrium / cavoatrial junction |
| Left internal jugular | 20–24 cm | Right atrium / cavoatrial junction |
| Femoral vein | ≥24 cm | Inferior vena cava, above the iliac confluence |
| Subclavian (avoid) | As for jugular | Cavoatrial junction |
Recirculation by site: internal jugular ≈ 10% (5–15%); femoral ≈ 20% (5–38%), worst with short catheters; reversing the lines to rescue flow pushes recirculation to 20–30%.
100 CRRT patients, 20–24 cm vs 15–20 cm catheters in a great thoracic vein: the longer catheter prolonged filter survival by a mean 6.5 h, delivered more dialysis dose and caused fewer clotting episodes (2.3 vs 3.6 per patient).
Morgan D et al. Am J Kidney Dis. 2012;60:272–279 · Ronco Ch 167 (recirculation) · Koyner Ch 29 Table 29.1
PlanSite, length, platelets/INR, and a pre-scan for thrombus or a collapsed vein. Mark the side you are preserving.
BarrierHand hygiene, cap, mask, sterile gown and gloves, full-body drape, >0.5% chlorhexidine in alcohol, allowed to dry.
Real-time ultrasoundNeedle tip visualised into the vein — fewer passes, fewer arterial punctures, fewer haematomas and pneumothoraces.
ConfirmAspirate and flush both lumens freely, then chest radiograph for a thoracic tip before the first treatment.
Real-time ultrasound guidance is the standard of care for dialysis catheters, not an option for difficult patients. Landmark insertion is now a documented deviation.
Rabindranath KS et al. Cochrane Database Syst Rev. 2011;(11):CD005279 · O'Grady NP et al. Clin Infect Dis. 2011;52:e162 · Koyner Ch 29 Table 29.2
In one cohort of temporary haemodialysis catheters, more than half had to be removed because of a complication rather than because they were no longer needed. Assume the line will cause a problem and plan its exit on the day you insert it.
Kairaitis LK, Gottlieb T. Nephrol Dial Transplant. 1999;14:1710 · Clark E et al. Can J Kidney Health Dis. 2016;3:2054358116669128 · Koyner Ch 29
Define it — cannot sustain the prescribed blood flow, or arterial pressure more negative than about −250 mmHg / venous pressure above about +250 mmHg at target flow. Rising transmembrane pressure is a filter problem, not an access problem.
Position first — hip flexion with a femoral line, head turn, a tip that has migrated up the SVC, a kink under the dressing. Free, instant, and the commonest cause.
Volume — a hypovolaemic patient collapses the vein around the arterial lumen. Look at the patient before you blame the catheter.
Reverse the lines only as a bridge — it buys flow at the cost of 20–30% recirculation and a silent loss of dose. Document it; do not normalise it.
Thrombolytic lock — alteplase dwell for suspected intraluminal thrombus before considering exchange.
Exchange or resite — guidewire exchange with new sterile gloves and a new field if uninfected; a new site if infection is suspected or the vein is thrombosed.
Ronco Ch 167 · Koyner Ch 29 · Clark E et al. Can J Kidney Health Dis 2016
Lopez-Briz E et al. Cochrane Database Syst Rev. 2018;7:CD008462 · Zhao Y et al. Am J Kidney Dis. 2014;63:479 · Polaschegg HD, Sodemann K. Nephrol Dial Transplant. 2003;18:2688 · CDC scrub-the-hub protocol · Koyner Ch 29
Subclavian catheterisation causes central venous stenosis far more often than jugular access — in the classic angiographic series, 42% vs 10%. A stenosis is silent until the day the arm swells after a fistula is created, and by then the whole limb is unusable. It is also the one site you cannot compress when a coagulopathic patient bleeds. If a subclavian is unavoidable, KDIGO advises using the dominant side.
Vein preservation is a whole-hospital behaviour: no PICC lines, no routine cannulation and no venepuncture in the non-dominant forearm of any patient who might need a fistula — which includes anyone with CKD 4–5, anyone dialysis-dependent, and anyone whose AKI may not recover. Put the sign on the bed on day one, not on the day you consult vascular surgery.
Schillinger F et al. Nephrol Dial Transplant. 1991;6:722 · Hernández D et al. J Am Soc Nephrol. 1998;9:1507 · KDIGO 2012 · Koyner Ch 29
No modality has ever been shown to save more lives than another — so choose the one whose physics matches the problem you are trying to solve.
Pilot RCT of CVVH vs CVVHD in critically ill AKI: convection was associated with a lower vasopressor requirement but no survival difference. A meta-analysis of 19 randomised comparisons of haemofiltration vs haemodialysis found no difference in mortality or any clinical outcome. Pick the mechanism that suits the circuit, not the survival curve.
Neri M et al. Crit Care. 2016;20:318 (ADQI standardised nomenclature) · Wald R et al. Crit Care. 2012;16:R205 · Friedrich JO et al. Crit Care. 2012;16:R146 · Koyner Ch 32 · Ronco Ch 176–177
| Mechanism | Driving force | Clears | Falls off when |
|---|---|---|---|
| Diffusion | Concentration gradient across the membrane | Small solutes <500 Da — urea, creatinine, potassium, bicarbonate | Molecular weight rises: clearance falls steeply above ~1 kDa |
| Convection | Transmembrane pressure dragging solvent, and solute with it | Small and middle molecules 500–5000+ Da — β₂-microglobulin, cytokines, myoglobin | The membrane's cut-off is reached, or protein layering blocks pores |
| Ultrafiltration | Hydrostatic pressure | Plasma water — solutes only incidentally | It is the only mechanism running (SCUF): no solute control at all |
| Adsorption | Binding to the membrane surface and pores | Some hydrophobic peptides and proteins | Sites saturate within hours — minor in routine CRRT |
Ronco Ch 165 · Brunet S et al. Am J Kidney Dis. 1999;34:486 · Koyner Ch 32
Uchino S et al. Nephron Clin Pract. 2003;94:c94 · Ronco Ch 165 · Koyner Ch 32 (Figure 32.1)
| Dimension | CRRT | IHD |
|---|---|---|
| Haemodynamic tolerance | Best — ultrafiltration spread over 24 h | Worst — the whole fluid target in 3–4 h |
| Net ultrafiltration control | Hourly, adjustable, matched to inputs | Intermittent and bolus-like; balance drifts between sessions |
| Solute control | Low hourly clearance, near steady state | High hourly clearance, peak-and-trough with rebound |
| Intracranial pressure / osmolar stability | Stable — the reason it is preferred in brain injury | Rapid urea fall risks osmotic shift and raised ICP |
| Anticoagulation | Usually required — regional citrate preferred | Often none or a short heparin course |
| Rapid removal of a toxin or of potassium | Slow | The correct tool |
| Mobility, physiotherapy, theatre and imaging | Tethered to the machine | Free between sessions |
| Nursing model | ICU nurse, one-to-one, 24 h | Dialysis nurse for the session |
| Nutrition and blood-product volume | Unlimited — space is created continuously | Constrained between sessions |
| Drug clearance | Continuous; antibiotic dosing must be re-thought (Lecture 9) | Intermittent; post-dialysis dosing |
| Cost and consumables | High | Lower |
Koyner Ch 32 Tables 32.2 and 32.4 · Ronco Ch 166 · KDIGO 2012 Section 5
360 patients with AKI and multiorgan failure randomised to CVVHDF vs IHD, with protocolised tolerance measures in the IHD arm: no difference in 60-day survival. Well-delivered IHD is safe in sick patients if you protect the blood pressure.
252 patients randomised to continuous vs intermittent KRT: no difference in survival, ICU stay or kidney recovery. Randomised data have never reproduced the recovery advantage seen in observational cohorts.
CRRT is chosen for control — of pressure, of volume, of osmolality — not for survival. Observational studies favouring CRRT for kidney recovery are confounded by indication: the unstable patient gets CRRT and the unstable patient recovers less. And practice varies far more than case mix does — CRRT was the initial modality in 80% of KRT starts across 54 ICUs in 23 countries in BEST Kidney, with wide between-country spread. When practice varies that much and outcomes do not, defend the delivery, not the acronym.
Vinsonneau C et al. Lancet. 2006;368:379–385 · Schefold JC et al. Crit Care. 2014;18:R11 · Schneider AG et al. Intensive Care Med. 2013;39:987 · Uchino S et al. JAMA. 2005;294:813 (BEST Kidney) · Koyner Ch 32
KDIGO 2012 · Lund A et al. Acta Anaesthesiol Scand. 2019;63:493 · Regolisti G et al. Nephrol Dial Transplant. 2013;28:79 · Koyner Ch 32
In most institutions PIRRT substitutes for CRRT, not for IHD — it is the step-down that keeps the haemodynamic profile while returning the patient's day.
232 critically ill patients with AKI randomised to SLED vs CVVH: 90-day mortality 49.6% vs 55.6% (not significant), with shorter mechanical ventilation, shorter ICU stay and less nursing time in the SLED arm. Single centre, and the CVVH arm was dosed near 31 mL/kg/h. A meta-analysis of seven RCTs found no mortality difference.
Schwenger V et al. Crit Care. 2012;16:R140 · Zhang L et al. Am J Kidney Dis. 2015;66:322 · Kumar VA et al. Am J Kidney Dis. 2000;36:294 · Koyner Ch 32
Chionh CY et al. Clin J Am Soc Nephrol. 2013;8:1649 (24 studies, 4 RCTs — no mortality difference vs extracorporeal KRT) · Cullis B et al. Perit Dial Int. 2014;34:494 (ISPD) · Phu NH et al. N Engl J Med. 2002;347:895 · Koyner Ch 32 · Ronco Ch 179, 183–186
Is there a life-threatening indication that needs speed? Refractory hyperkalaemia or a dialysable toxin → IHD now, whatever the blood pressure, then reassess.
Is the patient vasopressor-dependent, brain-injured or grossly overloaded? → CRRT, with the dose and anticoagulation strategy from Lecture 9.
Is volume the only problem, with acceptable chemistry? → SCUF, or a diuretic strategy first — do not start solute clearance you do not need.
Is the patient stabilising, or does the day need to be free? → SLED / PIRRT overnight as the step-down.
Stable, mobilising, chemistry controlled between sessions? → IHD thrice weekly at Kt/V 1.3; more frequent treatment has not improved outcomes and may impair recovery.
No safe vascular access, no machine, or no anticoagulation possible? → acute PD, provided the abdomen and the catabolic rate allow it.
Modality is not a one-time decision. It is a prescription reviewed daily and expected to change — CRRT to SLED to IHD is the normal trajectory of a recovering patient, and going backwards is not a failure. Local expertise, nursing ratios and machine availability are legitimate inputs; what actually changes outcome is a working access, a delivered dose and a circuit that stays alive.
KDIGO 2012 · Vijayan A et al. Kidney Int Rep. 2018;3:456 (frequency and recovery) · Koyner Ch 32
Four large randomised trials asked whether starting earlier helps; the consistent answer is that it does not, and that starting later has a floor.
| Indication | Working threshold | |
|---|---|---|
| A | Acidaemia | pH ≤7.20 or bicarbonate ≤12 mmol/L, refractory to ventilation and buffer — the STARRT-AKI trigger |
| E | Electrolytes | Potassium ≥6.0 mmol/L refractory to medical therapy, or any level with ECG change; also tumour lysis and severe refractory hypercalcaemia |
| I | Intoxication | A dialysable toxin — toxic alcohols, lithium, salicylate, valproate, metformin-associated lactic acidosis (EXTRIP recommendations) |
| O | Overload | Pulmonary oedema refractory to diuretics; STARRT-AKI used PaO₂/FiO₂ ≤200 judged to be volume-related |
| U | Uraemia | Encephalopathy, pericarditis or bleeding — clinical, not a number. AKIKI's delayed arm used blood urea nitrogen >112 mg/dL as one trigger |
In the presence of any of these, refractory to medical therapy, there is no debate and no trial — start, provided KRT is consistent with the patient's goals of care.
KDIGO 2012 · STARRT-AKI Investigators. N Engl J Med. 2020;383:240 · Gaudry S et al. N Engl J Med. 2016;375:122 · Koyner Ch 31 · Ronco Ch 163
Not "does this patient meet an indication?" but: is the metabolic and volume demand exceeding this kidney's remaining capacity, and for how many more hours can medical therapy hold the line? That is answerable at the bedside every morning.
Mehta RL. Blood Purif. 2001;19:227 · Bagshaw SM et al. Clin J Am Soc Nephrol. 2019;14:496 · Koyner Ch 31 · Ronco Ch 163
Population: 231 patients, single centre in Germany, mostly surgical (about half cardiac surgery), KDIGO stage 2 plus sepsis, refractory overload, worsening SOFA or vasoactive support. Comparison: KRT within 8 h of stage 2 vs at stage 3 or a conventional indication; CRRT mandated in both arms. Result: 90-day mortality 39.3% vs 54.7% (p = 0.03), median separation only 21 h. Interpretation: a real result in a narrow surgical population at one centre — hypothesis-generating, never replicated.
Population: 620 patients, 31 French ICUs, KDIGO stage 3 on ventilation and/or vasopressors, no life-threatening complication; two-thirds septic shock. Comparison: KRT within 6 h of stage 3 vs deferral until oliguria >72 h, urea nitrogen >112 mg/dL, hyperkalaemia, acidosis or pulmonary oedema. Result: 60-day mortality 48.5% vs 49.7% (HR 1.03, 95% CI 0.82–1.29). 49% of the delayed arm never received KRT at all; the early arm had more catheter-related bloodstream infection and more hypophosphataemia. Interpretation: half of the patients you were about to dialyse do not need it.
Zarbock A et al. JAMA. 2016;315:2190–2199 · Gaudry S et al. N Engl J Med. 2016;375:122–133 · Koyner Ch 31 Table 31.1
Population: 488 patients with septic shock and stage 3 AKI, 29 French ICUs. Comparison: KRT within 12 h of stage 3 vs after 48 h of persistent AKI or an emergent indication. Result: stopped early for futility; 90-day mortality 58% vs 54% (p = 0.38). 97% of the early arm received KRT vs 62% of the delayed arm, and most of those who never started recovered spontaneously. Interpretation: the sepsis-specific "early support" hypothesis fails on its own ground.
Population: 3019 randomised across 168 centres in 15 countries, stage 2–3 AKI, enrolled only where the attending physician confirmed genuine equipoise. Comparison: accelerated start within 12 h vs a standard strategy that discouraged KRT unless K ≥6.0, pH ≤7.20, bicarbonate ≤12 or volume-related PaO₂/FiO₂ ≤200 supervened. Result: 90-day mortality 43.9% vs 43.7% (RR 1.00, 0.93–1.09), consistent across every prespecified subgroup. Among survivors, dialysis dependence at 90 days was 10.4% vs 6.0% (RR 1.74, 1.24–2.43), and adverse events were more common with acceleration (23% vs 16.5%, mainly hypotension and hypophosphataemia).
Barbar SD et al. N Engl J Med. 2018;379:1431–1442 · STARRT-AKI Investigators. N Engl J Med. 2020;383:240–251 · Koyner Ch 31
Population: 278 patients who had already reached the AKIKI delayed-strategy threshold — oliguria beyond 72 h or urea nitrogen 112–140 mg/dL — with no emergent indication. Comparison: start now ("delayed") vs wait further until urea nitrogen exceeded 140 mg/dL or an emergency appeared ("more delayed"). Result: no gain in days alive and free of KRT; 60-day mortality was numerically higher in the more-delayed arm, and in adjusted analysis the more-delayed strategy was associated with an increased hazard of death. Interpretation: deferral is not a free option that can be extended indefinitely.
Between the ELAIN ceiling and the AKIKI-2 floor lies a wide, flat therapeutic window. Within it, the timing of the start does not determine the outcome — but having a written trigger list and a daily review does, because it is what keeps you inside the window.
Gaudry S et al. Lancet. 2021;397:1293–1300 (AKIKI-2) · Koyner Ch 31
| Write this in the notes | Threshold |
|---|---|
| Potassium | ≥6.0 mmol/L, or rising despite medical therapy, or ECG change |
| Acid–base | pH ≤7.20 or bicarbonate ≤12 mmol/L without a correctable cause |
| Oxygenation | PaO₂/FiO₂ ≤200 attributable to volume, or refractory pulmonary oedema |
| Cumulative balance | >10% of body weight and diuretic-unresponsive |
| Uraemia | Encephalopathy, pericarditis or bleeding |
| Duration | Oliguria beyond 72 h with no sign of recovery → escalate the review, do not simply keep waiting |
STARRT-AKI N Engl J Med 2020;383:240 · Gaudry S et al. Lancet 2021;397:1293 · KDIGO 2012 · Koyner Ch 31
These tools move the probability that this kidney will recover. They do not answer the question the trials asked, which is whether acting on that probability earlier helps — and it did not.
Chawla LS et al. Crit Care. 2013;17:R207 · Koyner JL et al. J Am Soc Nephrol. 2015;26:2023 · Klein SJ et al. Intensive Care Med. 2018;44:323 · Koyner Ch 16, 31
Fluid accumulation at KRT initiation and at KRT cessation both track mortality; the adjusted odds of death associated with fluid overload at cessation were around 2.5 in the PICARD cohort. "We are watching" is not a defence when the cumulative balance has crossed 10% of body weight and the patient is on 60% oxygen. Diurese, restrict, and if you cannot, start.
Watchful waiting without a written trigger list, a daily documented review and a ready access plan is not the strategy the trials tested — it is drift. The delayed arms of AKIKI, IDEAL-ICU and STARRT-AKI were protocolised, monitored, and had a defined point at which they acted.
Bouchard J et al. Kidney Int. 2009;76:422–427 · Ronco Ch 163 · Koyner Ch 31
The literature on when to stop is thin and largely empiric — which makes the few validated signals worth knowing precisely.
Every extra day is another day of catheter risk, anticoagulation, hypophosphataemia, drug removal and immobility. And repeated intradialytic hypotension delivers fresh ischaemic hits to a kidney that is trying to repair — the plausible mechanism behind the extra dialysis dependence seen with accelerated initiation in STARRT-AKI.
Uchino S et al. Crit Care Med. 2009;37:2576 · Palevsky PM et al. N Engl J Med. 2008;359:7 (ATN) · Ronco Ch 144 · Koyner Ch 31, 51
Stop taking fluidSet net ultrafiltration to zero once the patient is at target volume and see whether balance holds on diuretics alone.
Step down the intensityCRRT → SLED overnight → alternate-day IHD, guided by chemistry, not by the calendar.
Space the treatmentsExtend the interval as urine output and pre-treatment chemistry allow; measure a timed clearance if you are unsure.
Hold and observeStop while the patient is still in hospital and watch for 48–72 h. Resuming is easy; restarting from a ward bed at 2 a.m. is not.
Keep the catheter until the hold has clearly succeeded — then remove it the same day. Space treatments closely enough that no single session has to remove a large volume. Feed the patient adequately throughout; and remember that 6–10% of survivors remain dialysis-dependent at 90 days, so every discharge needs a nephrology follow-up plan (Lecture 9).
Ronco Ch 144 · STARRT-AKI N Engl J Med 2020;383:240 · Koyner Ch 51
"Can we dialyse this patient?" is a technical question with an easy answer; "should we?" is the one that needs a structure.
Baseline kidney function · comorbidity burden · functional and nutritional status · capacity and advance directives · what matters more, quality or length of life · is this patient a plausible long-term dialysis candidate?
Kruser JM et al. Ann Am Thorac Soc. 2017;14:426 · Wachterman MW et al. JAMA Intern Med. 2019;179:987 · Bagshaw SM et al. Clin J Am Soc Nephrol. 2019;14:496 · Koyner Ch 56 Box 56.1
PrepareICU team, nephrology and consultants agree the prognosis, what KRT can plausibly achieve, and the milestones that would count as success.
CommunicateAsk–Tell–Ask. Share the estimate, elicit values, propose KRT explicitly as a trial with a defined end point and a date.
ConductDeliver full therapy. Review progress against the agreed milestones daily and update the family — no silent drift.
ConcludeMeet on the agreed date. Met → continue. Partly met → negotiate a new trial. Not met → move to comfort-focused care as agreed at step 2.
Scherer JS, Holley JL. Clin J Am Soc Nephrol. 2016;11:344 · Renal Physicians Association. Shared Decision-Making in the Appropriate Initiation of and Withdrawal from Dialysis. 2nd ed. 2010 · Koyner Ch 56
Renal Physicians Association guideline (2nd ed, 2010) Table 56.2 · Chong K et al. Clin J Am Soc Nephrol. 2017;12:1744 · Koyner Ch 56 · Ronco Ch 148
Three referrals, three different questions: when, which, and whether.
66 M, community-acquired pneumonia, ICU day 3. Norepinephrine weaning, lactate normalised, ventilated on FiO₂ 0.4. Loop diuretic infusion started 12 h ago with little effect.
Start kidney replacement therapy today, or not?
Hands up · answer on the next slide
Write triggersK ≥6.0 · pH ≤7.20 · HCO₃ ≤12 · P/F ≤200 from volume · refractory oedema
Optimise nowStop nephrotoxins, review every infused volume, escalate or stop the diuretic on evidence
TestFurosemide stress test if the trajectory is unclear; a flat response means prepare, not start
Review dailyDocument the decision — including the decision not to start, and why
AKIKI: 49% of the delayed arm never needed KRT. STARRT-AKI: identical mortality, and 10.4% vs 6.0% dialysis dependence at 90 days favouring the standard strategy. AKIKI-2: but do not extend the wait past the point where an emergency is the only thing that will make you act.
Gaudry S et al. N Engl J Med 2016;375:122 · STARRT-AKI N Engl J Med 2020;383:240 · Gaudry S et al. Lancet 2021;397:1293 · Chawla LS et al. Crit Care 2013;17:R207
27 M, day 4 after a motorcycle collision. Decompressive craniectomy, ICP monitored, on hypertonic saline and mannitol. Rhabdomyolysis-associated AKI, now anuric. Ventilated, noradrenaline 0.15 µg/kg/min.
Which modality, and what are the two numbers you must protect?
Think 45 seconds — name the modality and the two targets
84 M, CKD stage 4 (baseline creatinine 2.8 mg/dL), moderate dementia, dependent for washing and dressing, three admissions this year for fluid overload. Admitted with aspiration pneumonia and shock; now ventilated, on two vasopressors, oliguric for 30 h. No advance directive. The family asks you to "do everything".
What do you offer, and how do you say it?
Four patients with KDIGO stage 3 AKI are on your list this morning. Which one should start KRT today?
A. pH 7.28, K 5.5, urine 0.3 mL/kg/h, balance +1 L, no oedema · B. K 6.4 with peaked T waves, unchanged after insulin–dextrose and salbutamol · C. Urea nitrogen 105 mg/dL, alert, eating, balance neutral · D. Oliguric 40 h, creatinine still rising, otherwise well and improving off vasopressors
Hands up — then name the trigger that fired
References & further reading
Questions & discussion — tomorrow we prescribe the therapy we have just decided to give.
Next: Lecture 09 — KRT II: Dose, Anticoagulation, Complications & Recovery