Acute Kidney Injury Ajay Dhaygude
Admitting specialty
Inadequate risk assessment
Missed complications
AKI vs ACS • Cardiac muscle Vs Pre, intra and post AKI • Rapidity & symptoms • Biomarker[s]
Relationship between GFR and Serum creatinine
Epidemiology • UK data 172 to 630 pmp/yr • AKI requiring dialysis: 200 pmp/year • ICU national audit: 4.9% patients have AKI and 10% bed days are accounted for AKI • Mortality: uncomplicated- 10% with MOF: 50% With RRT: 80% • Financial implications- £ 450-600 million/yr (more than Skin, breast and lung cancer treatment together)
Definition and stages • Serum creatinine rises by ≥ 26.5 μmol/L within 48 hours or • Serum creatinine rises ≥ 1.5 fold from the reference value, which is known or presumed to have occurred within one week or • urine output is < 0.5ml/kg/hr for >6 consecutive hours • Stage 1: 1.5 to 1.9 times raised S Cr. • Stage 2: 2 to 2.9 times raised S Cr. • Stage 3: S Cr more than 3 times high or absolute increase by 353 m mol/lr OR need to start dialysis
Selby et al PLoS One. 2012; 7(11): e48580.
Risk factors
Case-1 • JW-83 Yrs old, back ground, CKD, IHD • Admitted with Cl diff diarrhoea. • Inspite of oral vancomycin + rehydration developed AKI • Ref by ITU cons at CDH: • Decreased UOP (?). BP 110 systolic, apyrexial • Urea- 24.9, K- 4.6, Creat 423, (CRP improving) • pH 7.2, base excess -11, bicarb 15 • Pt has received 6 litres fluid in last 48 hours now RR 18, basal crackles, gases okay
Results
• How do you treat him? • ?diuretics • Urgent dialysis • Anything else
Diuretics in AKI, Bagshaw et al • 67% clinicians use diuretics in AKI • 86% patients had pulmonary oedema • IV Furosemide was most commonly used drug • Most clinicians were aware of toxicity, effect on renal recovery. • Most were willing to take part in RCT
Diuretics in AKI • Use if: – Fluid overloaded – Not hypotensive (?) • Use single large dose [up to 250 mg iv over 4 hours] • If no response then abandon further use • Monitor electrolytes/ fluid balance • Can enhance gentamicin toxicity • Diuretics does not cure AKI !!!
Case-2 • LH- 53 years young previously fit and well female patient is admitted with sudden onset severe abdominal pain. • On admission found to be confused, hypotensive • Rapid deterioration requiring ventilation and inotropic suport.
How will you investigate her? • CT abd excluded ischaemic bowel.
Biochemistry
Transferring patients with AKI • Death during transfer should be avoided at any cost • Get your critical care team involved if your patients has- – Severe acidosis, – refractory hyperkalemia, – haemodynamically unstable patients and severe pulmonary oedema
Cause of death in AKI, Selby et al
Sepsis and the critically ill Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock Emanuel Rivers, M.D., M.P.H., Bryant Nguyen, M.D., Suzanne Havstad, M.A., Julie Ressler, B.S., Alexandria Muzzin, B.S., Bernhard Knoblich, M.D., Edward Peterson, Ph.D., Michael Tomlanovich, M.D., for the Early Goal-Directed Therapy Collaborative Group Volume 345 : 1368-1377 November 8, 2001
Protocol group
Treatment given 0-6 hours 7-72 hours 0-72 hours EGDT 4991 8625 13443 Fluids (ml) Standard 3499 10602 13358 P value <0.001 0.01 0.73 EGDT 64.1 11.1 68.4 RBC transfusion Standard 18.5 32.8 44.5 (%) P value <0.001 <0.001 <0.001 EGDT 27.4 29.1 36.8 Vasopressor use Standard 30.3 42.9 51.3 (%) P value 0.62 0.03 0.02 EGDT 13.7 14.5 15.4 Dobutamine use Standard 0.8 8.4 9.2 (%) P value <0.001 0.14 0.15 EGDT 53.0 2.6 55.6 Mechanical Standard 53.8 16.8 70.6 ventilation (%) P value 0.90 <0.01 0.02
Electrolyte contents of some common fluids
Case-3 • IW- 70 Year old pt with H/O NHL is admitted with generalised oedema, and feeling unwell. • Finished chemotherapy 5 months ago, in remission. • O/E Gross oedema, hypotensive and tachypnoeic • CXR- Pulmonary oedema. • What investigations are needed?
Biochemistry
She is known to have severe biventricular failure due to valvular heart disease.
Management of cardio-renal syndrome • Diuretics Optimisation Strategies Evaluation trial: 308 pts low or high dose furosemide given as 12 hourly boli or continuous infusion. • No difference in infusion or bolus regime • High dose was associated with better response but higher likelyhood of renal impairment [23% vs 14%] • CARRESS-HF trial: compared haemofiltration versus stepped pharmacologic therapy. Later approach was superior.
Case-4 • AD, 79 yrs old male presented with haematuria and during hospital stay developed AKI
How would you investigate?
Missed investigations -NCEPOD
Case-5 • GB, 65 yr old pt with known CKD III was admitted with PR bleed. Sigmoidoscopy was normal but was found to have weight loss and was hospitalised. • Developed progressive AKI in hospital. Referred to medics • Also has purpuric rash, haematuria and haemoptysis. • CT chest- widespread nodular shadow, bronchoscopy- pulmonary haemorrhage. • Became anuric and was transferred to HDU for haemofiltration
How do you investigate further? • How do you manage this patient? • Urgent renal referral please.
Hyperkalaemia
Hyperkalaemia • Do an ECG + attach to cardiac monitor • 10ml 10% Calcium Gluconate; repeat until ECG normalizes • Nebulised Salbutamol (5-10mg) • 50ml 50% Dextrose + 10 unit Insulin • iv Sodium Bicarbonate (50-100ml 8.4% NaHCO 3 via central line) • Calcium Resonium (30g rectally)
Fluid overload Pulmonary Oedema • Furosemide 500mg iv over 1 hour • Oxygen • Opiates • Nitrate iv Dialysis if refractory to above Pericarditis • Pericarditis • More common in chronic renal failure than ARF • Risk of progression to tamponade
Acidosis Severe Acidosis • eg if pH <7.1 Symptomatic uraemia Symptomatic Uraemia • Confusion, coma, asterixis
Do’s and Don’ts Do I put in a central line? Only if uncertain of volume status Do I test the urine? Of course Do I use diuretic? Only for fluid overload Do I use Dopamine? No Do I give any other drugs? No Do I ask for urgent dialysis? If hyperkalaemia, fluid overload, pericarditis, acidosis
The take-home message • AKI is associated with significant mortality and has financial implications. • Elderly patients are at increased risk • Small rise in Creatinine suggests big drop n GFR • Sepsis is commonest cause of death • Remember acidosis!
Indications for Dialysis Persistent hyperkalaemia Fluid overload Pericarditis Acidosis Symptomatic uraemia
AKI= FLUIDS • F fluid balance • L low BP • U urine dipstics • I imaging • D drugs • S sepsis
Case -6 65Yr M. Admitted to BVH ITU with Creat 1100 H/o travel to Tenerife and developed some D&V PMH- Known single kidney (Creat 180- 3 months ago) USS ?Obstruction- nephrostomy- no Urine CT Pelvis- no cause for obstruction found Transferred to RPH- Immunology negative Kidney biopsy: crescentic GN+ Ischaemic changes + CPN Renal angio- RAS- Stented, antibiotics Remained on dialysis. Died after 6 months (line sepsis)
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