Acute Kidney Injury Ajay Dhaygude Admitting specialty Inadequate - - PowerPoint PPT Presentation

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 mmol/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

Early Goal-Directed Therapy in the Treatment

• f 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

Sepsis and the critically ill

Protocol group

Treatment given

0-6 hours 7-72 hours 0-72 hours Fluids (ml) EGDT 4991 8625 13443 Standard 3499 10602 13358 P value <0.001 0.01 0.73 RBC transfusion (%) EGDT 64.1 11.1 68.4 Standard 18.5 32.8 44.5 P value <0.001 <0.001 <0.001 Vasopressor use (%) EGDT 27.4 29.1 36.8 Standard 30.3 42.9 51.3 P value 0.62 0.03 0.02 Dobutamine use (%) EGDT 13.7 14.5 15.4 Standard 0.8 8.4 9.2 P value <0.001 0.14 0.15 Mechanical ventilation (%) EGDT 53.0 2.6 55.6 Standard 53.8 16.8 70.6 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% NaHCO3 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 I put in a central line? Do I test the urine? Do I use diuretic? Do I use Dopamine? Do I give any other drugs? Do I ask for urgent dialysis? Only if uncertain of volume status Of course Only for fluid overload No No If hyperkalaemia, fluid overload, pericarditis, acidosis

Do’s and Don’ts

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)