Acute kidney failure resident survival guide

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: Kanwal Khamuani, M.B.B.S.

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.

• Renal hypoperfusion due to abdominal aortic aneurysm
• Acute tubular necrosis
• Sepsis leading to hypotension

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.

Pre Renal Causes

• Hypovolaemia

• Haemorrhage
• Volume depletion(for example vomiting, diarrhea, burns, and inappropriate diuresis)

• Renal hypoperfusion

• Non-steroidal anti-inflammatory drugs/selective cyclo-oxygenase 2 inhibitors
• Angiotension converting enzyme inhibitors/angiotension receptor antagonist
• Abdominal aortic aneurysm
• Renal artery stenosis/occlusion
• Hepatorenal syndrome

• Hypotension

• Cardiogenic shock
• Distributive shock(for example sepsis, anaphylaxis)

• Oedematous States

• Cardiac failure
• Hepatic cirrhosis
• Nephrotic syndrome

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

• pelvic malignancy
• retroperitoneal fibrosis

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) ❑ 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 treatment rely upon the underlying cause; however, the initial approach is directed to manage any life-threatening feature in order to halt or reverse the decline of the renal function, and if unsuccessful, support is provided by renal replacement to aid recovery. Hyperkalemia, pulmonary edema, and severe acidosis require immediate attention. 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 at once treated with infusion of calcium. Infusion of calcium is a temporary management, therefore measures are started to decrease the serum potassium by increasing cellular uptake simultaneously. Overall these steps are enough to normalize the serum potassium; 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 can be started.

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

Excessive fluid therapy can lead to Pulmonary oedema, especially in patients with known cardiac dysfunction, the elderly, and those who were volume replete at the start—and can be prevented by judicious intravenous fluid therapy. If respiratory failure ensues, patient should be intubated and mechanical ventilation started. Simultaneouly, pharmacological treatment can be started to disburden the decompensated heart. If these measures fail, hemodialysis or hemofiltration can be used.

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

Variety of mechanisms can cause severe metabolic acidosis (blood pH <7.2) in patients with ARF either due to reduced renal function or due to underlying cause of the patient's illness. Systemic acidosis diminishes cardiac contractility, induces bradycardia, develop vasodilatation, and further expands hyperkalemia. Although there is very little known benefit, Alkaline solution-sodium bicarbonate is administered to reverse acidosis. 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 needed. Haemodialysis or haemofiltration will usually be required to treat severe acidosis in oligoanuric patients.

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.
• Do not use dopamine to increase renal perfusion.
• Cautiously use diuretics if oliguria persists.
• Do not use nephrotoxic drugs (NSAIDs, ACE-I, Aminoglycosides)
• Avoid use of contrast media.

References