Acute Kidney Injury Flashcards
(31 cards)
What is acute kidney injury (AKI)?
This is an acute decline in renal function, leading to a rise in serum creatinine and/or a fall in urine output.
Kidney injury presents a disease spectrum from mild renal impairment to severe renal failure.
What is AKI most commonly associated with?
Sepsis Cardiovascular collapse CHF Major surgery Nephrotoxins (antibiotics, IV contrast) Urinary outflow obstruction
How does AKI present?
Flank pain Decreased urine output HTN or hypotension Oedema Lethargy Uraemia It is however often asymptomatic
What is essential for the diagnosis of AKI?
An acute increase in serum creatinine is essential for diagnosis. Fluid overload Hyperkalaemia Hyperphosphataemia Metabolic acidosis Elevated urea nitrogen
What is the mainstay of AKI treatment?
Supportive care: Management of the underlying illness Correction of acid/base electrolyte and volume complications Removal or minimisation of nephrotoxins Relief of any associated obstruction
Aetiology of AKI
Aetiology of AKI is generally classified into pre-renal, intrinsic and post-renal causes
Pre-renal causes of AKI
Causes of reduced renal perfusion: Hypovolaemia Haemorrhage Sepsis The third spacing of fluid (such as in severe pancreatitis) Overdiuresis Heart failure Hepatorenal syndrome Renovascular disease esp. with the recent addition of an ACE inhibitor to a patient with bilateral renal artery stenosis.
Intrinsic causes of AKI
ATN, rapidly progressive glomerulonephritis and interstitial nephritis are the most common aetiologies. Vascular diseases: Haemolytic uraemic syndrome Thrombotic thrombocytopenic purpura Scleroderma renal crisis Atheromatous embolisation Thrombosis 10% of intrinsic AKI causes are NSAIDs, ACEi, ARBs, gentamicin, vasculitis, myeloma, rhabdomyolysis and interstitial nephritis.
Post-renal causes of AKI
Mechanical obstruction of the urinary outflow tract. Retroperitoneal fibrosis Lymphoma Tumour Prostate hyperplasia Strictures Renal calculi Ascending urinary infection (including pyelonephritis) Urinary retention
Pathophysiology of AKI
Pre-renal azotaemia results from impaired renal perfusion and the changes seen are appropriate physiological responses.
The renal response is a lower perfusion pressure to enhance sodium and water re-absorption.
Baroreceptors in the carotid artery and aortic arch respond to lower BP with sympathetic stimulation.
This maintains glomerular filtration within a relatively narrow range.
History in pre-renal failure
Excessive fluid loss from haemorrhage.
GI tract-vomiting, diarrhoea.
Sweating.
Symptoms of hypovolaemia: thirst, dizziness, tachycardia, oliguria or anuria.
Hx of sepsis, burns, GI surgery or pancreatitis.
History in post-renal failure
More common in older men with prostatic obstruction.
Hx of urgency, frequency or hesitancy.
Hx of malignancy, prostatism, nephrolithiasis or previous surgery may coincide with the diagnosis of obstruction.
Obstruction caused by renal calculi or papillary necrosis typically presents with flank pain and haematuria.
Hx in intrinsic renal disease
ATN subsequent to severe infection, nephrotoxic drug exposure, or major surgery.
Hx of rash, haematuria or oedema with HTN suggesting nephritic syndrome and acute glomerulonephritis or renal vasculitis.
Hx of myeloproliferative disorder such as multiple myeloma may predispose to AKI.
Hx of all current medicines should be taken to establish any exposure to potential nephrotoxins.
Pigment-induced AKI due to rhabdomyolysis should be suspected in patients presenting with muscle tenderness, seizures, drug abuse or alcohol abuse, excessive exercise or limb ischaemia (e.g. from crush injury)
Physical examination findings in a patient with AKI
Hypotension, HTN, pulmonary oedema or peripheral oedema may be present.
There may be asterixis or altered mental status when uraemia is present.
Patients with fluid loss, sepsis or pancreatitis may have hypotension.
Patients with the glomerular disease typically present with HTN and oedema, proteinuria and microscopic haematuria (nephritic syndrome)
The presence of rash, petechiae or ecchymoses may suggest an underlying systemic condition such as vasculitis, thrombotic microangiopathy or glomerulonephritis.
An underlying abnormal bruit may support renovascular disease.
Patients with ATN may present after haemorrhage, sepsis, drug overdose, surgery, cardiac arrest or other conditions associated with hypotension and prolonged renal ischaemia.
Investigations of AKI
Basic metabolic profile (including urea and creatinine) Venous blood gases FBC Urinalysis and culture dipstick Urine chemistries Renal ultrasound CXR-pulmonary oedema or cardiomegaly ECG- arrhythmias is hyperkalaemia is present
Differentials of AKI
CKD
Increased muscle mass
Drug side effect
Risk factors of AKI
Advanced age > 65 Underlying renal disease (acute or chronic) Malignant HTN DM Myeloproliferative disorders such as multiple myeloma Connective tissue disease. Sodium-retaining states (CCF, cirrhosis, nephrotic syndrome) Exposure to nephrotoxins (aminoglycosides, cancer therapies, NSAIDs, ACEi, ARBs and diuretics Radiocontrast Trauma Haemorrhage Sepsis Pancreatitis Drug overdose Surgery Cardiac arrest Excessive fluid loss Recent vascular intervention Nephrolithiasis Oliguria
Stages of AKI
There are 3 stages.
Stage 1:
Increase >26 umol/L within 48 hours or increase >1.5-1.9 * reference SCr
<0.5 ml/kg/hr for >6 consecutive hours.
Stage 2:
Increase >2-2.9* reference SCr
<0.5 ml/kg/hr for >12 consecutive hours.
Stage 3:
Increase >3* reference SCr
<0.3 ml/kg/hr for >24 consecutive hours or anuria for 12 hours.
General management of AKI
Treat the underlying illness.
Intervention in the electrolyte and acid/base abnormalities and optimisation of volume status either by fluid replacement or fluid removal in patients with volume overload.
Sodium and volume restriction is generally required along with limiting potassium and phosphorus intake.
Patients with AKI shouldn’t be given potentially nephrotoxic drugs unless there is no alternative.
Management of pre-renal failure
Managed with techniques to improve the haemodynamic status of the patient.
Hypovolaemia correction with crystalloid or colloid (but not HES)
Vasopressors are recommended if hypotension is severe.
Management is often difficult if renal hypoperfusion results from impaired cardiac function due to poor left ventricular systolic function.
RRT may be needed if severe acid/base electrolyte or uraemic complications are present while underlying cardiac or volume issues are treated.
Management of intrinsic failure
Varies according to aetiology.
Volume overload require sodium restriction.
Volume expansion is required when co-existing pre-renal azotaemia exists.
Acute glomerulonephritis and vasculitis may also require corticosteroids, cytotoxic agents or other immune-modifying drugs.
No specific treatment for ATN aside from maintaining volume status and controlling electrolyte levels
Management of obstructive renal failure
Bladder catheter placement
RRT may be required if indicated
Indications of RRT
Refractory severe hyperkalaemia Acidosis Volume overload Uraemia -Continuous RRT is required in haemodynamically unstable patients or those in whom aggressive ultrafiltration within the conventional 4-6 hour treatment of haemodialysis would not be tolerated.
What are the key points in a history and examination to cover with reference to a patient with an acute kidney injury?
AKI risk factors
People aged 65 years or over.
A history of acute kidney injury.
Chronic kidney disease (estimated glomerular filtration rate [eGFR] less than 60mL/min/1.73m2).
Symptoms or history of urological obstruction or conditions which may lead to obstruction.
Chronic conditions such as heart failure, liver disease, and diabetes mellitus.
Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer).
Sepsis.
Hypovolaemia.
Oliguria (urine output less than 0.5mL/kg/hour).
Nephrotoxic drug use within the last week (especially if hypovolaemic) — for example nonsteroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists (ARBs), and diuretics.
Exposure to iodinated contrast agents within the past week
