Acute kidney failure resident survival guide

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Acute kidney failure
Resident Survival Guide
Overview
Causes
Diagnosis
Treatment
Do's
Don'ts

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Synonyms and keywords: Acute renal failure approach, An approach to acute renal failure, Acute kidney injury workup algorithm, Acute kidney injury management algorithm

Overview

Acute Renal Failure is a sudden decrease in kidney function defined as at least one of the following: 1. a definite increase in the serum levels of creatinine of 26.4 μmol/L(0.3mg/dl) or more; 2. A proportion increase in the serum levels of creatinine of more than 50% (1.5 fold increase from baseline); or 3. A decrease in the volume of urine output (oliguria <0.5 ml/kg hourly for >6 hours. The majority of causes of in-hospital acute renal failure is acute tubular necrosis resulting from multiple nephrotoxic insults such as sepsis, hypotension, and use of nephrotoxic drugs or radio-contrast media. Patients at risk include elderly people, diabetics, patients with hypertension or vascular disease, and those with pre-existing renal impairment.To aid the diagnosis and management, it is important to find out the underlying cause; whether it is pre-renal, renal, or postrenal. Initial workup should be performed as soon as the patient is encountered and any life-threatening situation should be treated promptly.

Causes

Life Threatening Causes

Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.

Common Causes

 
 
 
 
 
 
 
 
Acute renal failure
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Pre-renal causes/Hypotension
 
 
 
 
Intrinsic renal causes
 
 
 
 
Post-renal causes/Obstructive causes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Glomerular disease
 
 
Tubular insult
 
 
 
 
Interestitial nephritis
 
 
Vascular causes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Ischemia
 
 
 
 
 
 
 
 
 
 
Inflammation (vasculitis)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Inflammation
 
 
 
Toxins
 
 
 
Oclusion (thrombosis or embolism
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Thrombosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
This algorithm developed and modified according to a clinical review published in BMJ.[1]

Pre Renal Causes

  • Oedematous States

Intrinsic Renal Causes

Post Renal Causes

  • Intrinsic
  • Extrinsic

Diagnosis

Shown below is an algorithm summarizing an step by step approach to diagnosis the cause of Acute Renal Failure to aid in the management.[2][1] Abbreviations: NSAIDs: Non-steroidal anti-iflammatory drugs; ACE: Angiotensin converting enzyme; ARF: acute renal failure; RRT: Renal replacement therapy; ATN:acute tubular necrosis; ECG:Electrocardiogram

 
 
 
 
 
 
Patient presenting features

Oliguria (sudden or gradual)
Anuria
Edema
Hypotension
Hematuria
Loin pain
Renal colic
Bone pain

Fever
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Medical History and Risk Factors

❑ inquire about previous similar episodes
❑ co-morbidities

Diabetes-long standing poorly controlled diabetes can precipitate ARF
Hypertension
Heart Failure
Vascular disease (such as renal artery stenosis

❑ Inquire about medication history

ACE inhibitors- can precipitate ARF in renal artery stenosis
NSAIDs-associated with interstitial kidney disease
Penicillins-associated with renal papillary necrosis

❑ inquire about recent hospitalization-rule out ATN
❑ Inquire about recent trauma/surgery-rule out sepsis-look for fever and hypotension/rule out hemorrhage and hypovolemia
❑ Age factor-elderly people-rule out Benign Prostate hypertrophy/prostate cancer

❑ Elderly patient with bone pain-Multiple Myeloma?

❑ History of kidney stones
❑ Associated symptoms

❑ Nasal stuffiness/epistaxis-suggest Wagener's Granulomatosis?
❑ recent sore throat-streptococcal Glomerulonephritis

❑ Social history-Alcohol use/tobacco use/drug abuse
❑ history of autoimmune disorders- Systemic Lupus Erythromatosus, Good Pasture syndrome

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Initial work-up

❑ Basic Blood

Full blood count with differentials
Blood glucose
Urea and electrolytes
Coagulation screen
❑ Inflammatory markers
❑ Urea/electrolytes
Liver function test
Calcium and phosphate
❑ Blood culture if infection suspected
❑ Arterial blood gases or venous bicarbonate

Urine analysis
❑ Urine microscopy/urine sediment/culture
❑ Renal ultrasound
❑ Chest radiograph
ECG
Renal biopsy may be indicated if intrinsic cause is suspected

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Draw a conclusion

❑ Treat any life threatening features first—shock, respiratory failure, hyperkalaemia
❑ Is this acute or chronic renal impairment?
❑ A full drug history (current, recent, and alternative medication) is vital
❑ Is there a pre‐renal cause? What is the patient's current fluid status?
❑ Could this be obstruction?
❑ Is intrinsic renal disease probable—what does urine analysis show?

 
 
 

Renal failure diagnostic approach
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is this acute or chronic renal failure
 
❑ History and physical examination
❑ Previous creatinin measurement
❑ Small kidneys on ultrasound except in diabetes
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Has obstruction been excluded?
 
❑ Complete anuria
❑ Palpable bladder
Renal ultrasound
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Is the patient euvolemic?
 
❑ Check pulse, JVP, orthostatic hypotension, daily weights, fluid balance
❑ Check for BUN/Cr ratio
❑ Check for urinary sodium
❑ Do fluid challeng test
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Does evidence of renal parenchymal disease exist? (other than ATN)
 
❑ History and physical examination (clinical features)
❑ Check urine dipstick and microscopy for RBC, WBC, and protein sodium
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Has a major vascular occlusion occurred?
 
❑ Ask for a history of atherosclerotic vascular disease
❑ Check for renal asymmetry
❑ Check for loin pain
❑ Check for macroscopic hematuria
❑ Check for complete anuria
 
 
 
 
 
 
 
 
 
 
 
 
 

Treatment

Definitive Management depends upon the underlying cause; however, the initial approach is directed to treat any life-threatening feature attempting to halt or reverse the decline of the renal function, and if unsuccessful providing support by renal replacement anticipating a renal recovery. Hyperkalemia, pulmonary edema, and severe acidosis require immediate attention.[2] Abbreviations: DDAVP: 1-deamino-8-D-arginine vasopressin; DVT: deep venous thrombosis; ARF: acute renal failure; RRT: Renal replacement therapy; I/V:Intravenous

1. HYPERKALEMIA TREATMEMT

Severe hyperkalemia is a medical emergency and should be immediately treated with infusion of calcium. Treatment with calcium is a temporizing measure “buying time” while measures are started to reduce the serum potassium through increasing cellular uptake. Overall these measures will bring the potassium back to normal; however, still, the body will be in excess. If pure pre-renal failure, measures can be taken to excrete the potassium through the kidney by giving resins. Ultimately, if hyperkalemia is refractory to all the above measures, hemodialysis ca be started.[2]

 
 
 
 
 
 
 
Serum potassium>6.5 is a medical emergency
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Immediate action
 
 
Reduction in plasma potassium concentration
 
 
Removal of potassium from the body
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Calcium gluconate or carbonate
 
 
 
 
 
 
 
 
If pure pre-renal failure, renal excretion will serve to return the whole body levels to normal
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
to stabilize the myocardium and prevent cardiac arrythmias
 
 
 
 
 
 
Ion exhange resins calcium polystrene or sodium polystrene
 
Hemodialysis for refractory hyperkalemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Insulin with glucose
 
beta-2 agonist
 
Sodium bicarbonate
 
 
 
 

2. TREATING PULMONARY EDEMA

Pulmonary oedema is often the result of excessive fluid resuscitation, and can be anticipated in many patients—especially those with known cardiac dysfunction, the elderly, and those who appear volume replete at the outset—and hopefully avoided by more judicious intravenous fluid therapy. If respiratory failure, intubate the patient and start mechanical ventilation.While these measures are being undertaken, pharmacological treatment to offload the decompensated heart can be started. If these measures fail, hemodialysis or hemofiltration can be used.[2]

 
 
 
 
 
 
 
 
PULMONARY EDEMA
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Respiratory failure
 
 
 
 
 
 
 
Pharmacological treatment
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
I/V opioids(diamorphine)
 
 
I/V infusion of glyceryl nitrate
 
provoke diuresis with large doses of diuretics such as furesemide
 
 
 
Supplemental oxygen OR intubate and mechanically ventilate
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

3. TREATING ACIDOSIS

Severe metabolic acidosis (blood pH <7.2) often accompanies ARF and arises through a variety of mechanisms, related both to reduced renal function and the underlying cause of the patient's illness. Systemic acidosis impairs cardiac contractility, induces bradycardia, produces vasodilatation, and augments hyperkalemia, among other effects. Reversing acidosis through the administration of an alkaline solution—sodium bicarbonate—would seem to be sensible, but there is very little evidence to show that it provides benefit. Isotonic (1.26%) solutions may have a role as fluid replacement therapy in stable patients with a moderate to severe acidosis and a requirement for fluid replacement, in whom dialysis is not imminent. Haemodialysis or haemofiltration will usually be required to treat severe acidosis in oligoanuric patients.[2]

4. OTHER GENERAL MEASURES


 
 
 
 
 
 
General Measures
❑ Fluid Balance-normal saline preferred but avoid fluid overload
❑ Relief of Obstruction-Bladder outflow obstruction if suspected should be relieved by passage of urethral catheter
Uremic Platelet Dysfunction-RRT may improve but DDAVP and cryoprecipitate may be required
Carbohydrate and protein requirement should be tailored individually and ideally delivered by enteral route
❑ Practice good infectious control
❑ Care of pressure areas
DVT prophylaxis if prolonged immobility
 
 
 
 
 
 
 
 
 
 
 

Do's

Don'ts

References

  1. 1.0 1.1 Hilton R (2006). "Acute renal failure". BMJ. 333 (7572): 786–90. doi:10.1136/bmj.38975.657639.AE. PMC 1601981. PMID 17038736.
  2. 2.0 2.1 2.2 2.3 2.4 Fry AC, Farrington K (2006). "Management of acute renal failure". Postgrad Med J. 82 (964): 106–16. doi:10.1136/pgmj.2005.038588. PMC 2596697. PMID 16461473.