Acute kidney failure resident survival guide
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 an abrupt reduction in kidney function defined as at least one of the following: 1. an absolute increase in the serum levels of creatinine of 26.4 μmol/L(0.3mg/dl) or more; 2. a percentage increase in the serum levels of creatinine of more than 50%(1.5 fold increase from baseline); or 3. a reduction in the volume of urine output(oliguria <0.5 ml/kg hourly for >6 hours. Acute renal failure is increasingly common, particularly in the elderly population, hospital inpatients, and critically ill patients and it carries a high mortality. The most common cause of in-hospital acute renal failure in 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 pre-existing renal impairment[1].To aid the diagnosis and management, it is important to find out the underlying cause, whether its pre-renal, renal, or postrenal. Initial workup should be carried out as soon as the patient is encountered and any life-threatening situation should be treated promptly.[2]
Causes
Life Threatening Causes
Life-threatening causes include conditions that may result in death or permanent disability within 24 hours if left untreated.
- Renal Hypoperfusion due to Abdominal aortic aneurysm
- Acute tubular necrosis
- Sepsis leading to hypotension
Common Causes
Acute renal failure | |||||||||||||||||||||||||||||||||||||||||||||
Pre-renal causes | Intrinsic renal causes | Post-renal causes | |||||||||||||||||||||||||||||||||||||||||||
Glomerular disease | Tubular injury | Interestitial nephritis | Vascular diseases | ||||||||||||||||||||||||||||||||||||||||||
Ischemia | Inflammation (vasculitis) | ||||||||||||||||||||||||||||||||||||||||||||
Inflammation (glomerulonephritis) | Toxins | Oclusion (thrombosis or embolism | |||||||||||||||||||||||||||||||||||||||||||
Thrombosis | |||||||||||||||||||||||||||||||||||||||||||||
Pre Renal Causes
- Hypovolaemia
- Haemorrhage
- Volume depletion(for example vomiting, diarrhea, burns, inappropriate diuresis)
- Renal Hypoperfusion
- Hypotension
- Cardiogenic shock
- Distributive shock(for example sepsis, anaphylaxis)
- Oedematous States
Intrinsic Renal Causes
- Glomerular disease
- Inflammatory- post-infectious glomerulonephritis, cryoglobulinaemia, Henoch-Schonlein purpura, systemic lupus erythematosus, antineutrophil cytoplasmic antibody associated glomerulonephritis, anti-glomerular basement membrane disease
- Thrombotic- disseminated intravascular coagulation, thrombotic microangiopathy
- Interstitial Nephritis
- Drug Induced- Non-steriodal anti-inflammatory drugs, antibiotics
- Infiltrative- Lymphoma
- Granulomatous- Sarcoidosis, Tuberculosis
- Infection related- post-infective, Pyelonephritis
- Tubular Injury
- Ischemia- prolonged renal hypoperfusion
- Toxins- drugs(such as aminoglycosides), radiocontrast media, pigments(such as myoglobin), heavy metals(such as cisplatinum)
- Metabolic- hypercalcemia, immunoglobin light chains
- Crystals- urate, oxalate
- Vascular
- Vasculitis(usually associated with antineutrophil cytoplasmic antibody)
- Cryoglobulinaemia
- Polyarteritis nodosa
- Thrombotic microangiopathy
- Cholesterol emboli
- Renal artery thrombosis/renal vein thrombosis
Post Renal Causes
- Intrinsic
- Intra-luminal- stone, blood clot, papillary necrosis
- Intra-mural- urethral stricture, prostatic hypertrophy or malignancy, bladder tumor, radiation fibrosis
- 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. 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) | |||||||||||||||||||||||||||||||||
Medical History and Risk Factors ❑ inquire about previous similar episodes
❑ Inquire about drug history
❑ inquire about recent hospitalization-rule out ATN
❑ history of kidney stones
❑ Social history-Alcohol use/tobacco use/drug abuse | |||||||||||||||||||||||||||||||||
Initial work-up ❑ Basic Blood
❑ Urine analysis | |||||||||||||||||||||||||||||||||
Draw a conclusion ❑ Treat any life threatening features first—shock, respiratory failure, hyperkalaemia | |||||||||||||||||||||||||||||||||
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? | |||||||||||||||||||||||||||||||||||||||||||
Is the patient euvolemic? | |||||||||||||||||||||||||||||||||||||||||||
❑ History and physical examination (clinical features) ❑ Check urine dipstick and microscopy for RBC, WBC, and protein sodium | |||||||||||||||||||||||||||||||||||||||||||
Has a major vascular occlusion occurred? | |||||||||||||||||||||||||||||||||||||||||||
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.[3] 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.[3]
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.[3]
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.[3]
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
- Normal Saline is the preferred fluid for resuscitation.
- Treat acute renal failure keeping in mind the cause behind it.
- Start Dialysis when needed.
- Correction of coagulopathy if needed with DDAVP and cryoprecipitate.
- DVT prophylaxis if needed.
- Avoid pressure ulcers.
Don'ts
- Avoid fluid overload.
- Dont use dopamine to increase renal perfusion.
- cautious use of diuretics if oliguria persists.
- Don't use nephrotoxic drugs (NSAIDs, ACE-I, Aminoglycosides)
- Avoid use of contrast media.
References
- ↑ "StatPearls". 2020. PMID 28722925.
- ↑ 2.0 2.1 2.2 2.3 Hilton R (2006). "Acute renal failure". BMJ. 333 (7572): 786–90. doi:10.1136/bmj.38975.657639.AE. PMC 1601981. PMID 17038736.
- ↑ 3.0 3.1 3.2 3.3 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.
- ↑ "StatPearls". 2020. PMID 28722925.
- ↑ 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.
- ↑ Hilton R (2006). "Acute renal failure". BMJ. 333 (7572): 786–90. doi:10.1136/bmj.38975.657639.AE. PMC 1601981. PMID 17038736.