🚨 Acute Kidney Injury

Acute Kidney Injury (AKI) is a sudden decline in renal function, leading to accumulation of waste products. Early recognition and management are crucial to prevent progression to chronic kidney disease or death, often precipitated by hypovolaemia, sepsis, or nephrotoxic drugs.

Recognise AKI by a rapid rise in serum creatinine (e.g., >26 micromol/L within 48 hours or >1.5 times baseline within 7 days) or a fall in urine output (<0.5 mL/kg/hour for >6 hours). Patients may present with oliguria, oedema, nausea, lethargy, or confusion. Consider risk factors like sepsis, hypovolaemia, heart failure, or pre-existing CKD.

Perform an ABCDE assessment, paying close attention to circulation (hypotension, tachycardia) and neurological status (confusion, reduced GCS). Assess for signs of fluid overload (pulmonary oedema, raised JVP) or dehydration (dry mucous membranes, reduced skin turgor). Check for bladder distension and catheter patency if applicable.

Red flags include severe oliguria/anuria, hyperkalaemia (especially with ECG changes), metabolic acidosis, pulmonary oedema, uremic encephalopathy, or cardiac tamponade. Any rapid deterioration in GCS, persistent hypotension despite fluid resuscitation, or new arrhythmias warrant urgent attention.

Bedside: Urinalysis (dipstick for protein, blood, leukocytes), urine output monitoring, ECG (for hyperkalaemia). Bloods: U&Es (creatinine, urea, electrolytes), FBC, LFTs, CRP, ABG (for acidosis). Imaging: Renal ultrasound (to assess for obstruction, kidney size) is often indicated.

Address the underlying cause, e.g., treat sepsis, restore circulating volume with intravenous fluids, or stop nephrotoxic drugs. Ensure adequate hydration, but avoid fluid overload in patients with established AKI. Manage hyperkalaemia with appropriate agents and acidosis with bicarbonate if severe. Consider urinary catheterisation for accurate output monitoring and to rule out obstruction.

Escalate to a senior registrar or consultant immediately for severe AKI (stage 3), hyperkalaemia with ECG changes, fluid overload unresponsive to diuretics, or suspected obstructive uropathy. Consider critical care referral for patients requiring renal replacement therapy or with multi-organ failure.

Prerenal AKI is the most common type, often due to hypovolaemia or reduced renal perfusion. Always review medication charts for nephrotoxic drugs (e.g., NSAIDs, ACE inhibitors). Postrenal AKI is often reversible with relief of obstruction. Remember the '3 Rs' of AKI: Recognise, Respond, Review.