Acute Kidney Injury: EMT Guide

Acute Renal Failure (Acute Kidney Injury): Emergency Assessment and Management

Why this topic matters: Acute kidney injury (AKI), historically called acute renal failure, is a sudden decline in kidney filtration over hours to days. It may be reversible, but untreated AKI can cause hyperkalaemia, metabolic acidosis, pulmonary oedema, uraemic encephalopathy, bleeding and death. Emergency providers must find reversible causes, assess volume carefully, stop nephrotoxins, monitor urine output and electrolytes, and involve renal/critical-care teams before complications become irreversible.

Learning objectives

Define AKI and classify pre-renal, intrinsic renal and post-renal causes.
Recognise oliguria, anuria, uraemia, hyperkalaemia, acidosis and fluid overload.
Perform ABCDE, fluid-status assessment, medication review and focused renal history.
Describe investigations, emergency treatment and indications for renal replacement therapy.
Plan nursing monitoring, prevention, referral, discharge education and follow-up.

Definition and pathophysiology

AKI is an abrupt reduction in kidney function, reflected by a rising serum creatinine, reduced urine output or both. The kidneys lose the ability to regulate water, electrolytes, acid-base balance and waste excretion. A patient may have severe AKI with few symptoms, so comparison with baseline creatinine and accurate urine measurement are essential.

Pre-renal AKI results from reduced renal perfusion such as haemorrhage, dehydration, sepsis, burns or heart failure. Intrinsic AKI involves the kidney tissue, including acute tubular injury, glomerulonephritis, interstitial nephritis, rhabdomyolysis or nephrotoxins. Post-renal AKI is obstruction from stones, prostate disease, clots, tumours, pregnancy or blocked catheters.

Safety point: Do not assume that reduced urine always means dehydration. Sepsis, obstruction, nephrotoxins and intrinsic renal disease may coexist. Give fluids only after a clinical volume assessment and reassessment of lungs, perfusion, BP and urine output.

Common causes and risk factors

Category	Examples	Clues
Reduced perfusion	Vomiting/diarrhoea, haemorrhage, burns, sepsis, shock, heart failure.	Hypotension, tachycardia, dry mucosa, low JVP or poor capillary refill.
Nephrotoxins	NSAIDs, aminoglycosides, contrast, amphotericin, some antivirals, herbal remedies and toxins.	Recent medicine or contrast exposure; rising creatinine after treatment.
Intrinsic renal disease	Glomerulonephritis, interstitial nephritis, tubular injury, vasculitis and rhabdomyolysis.	Haematuria/proteinuria, rash, eosinophilia, oedema or dark urine.
Obstruction	Stones, enlarged prostate, tumours, clots, pregnancy or blocked catheter.	Colicky pain, anuria, palpable bladder, hydronephrosis or poor catheter drainage.
High-risk patients	CKD, diabetes, hypertension, older age, pregnancy, children and major surgery.	Low renal reserve and higher risk from small physiological insults.

Triage and first contact

Move unstable patients to resuscitation and call senior emergency, renal and critical-care support.
Ask about urine output, baseline kidney function, fluid loss, fever, pain, obstruction, medicines, pregnancy and recent procedures/contrast.
Check for life-threatening hyperkalaemia, pulmonary oedema, severe acidosis, shock, uraemic encephalopathy and toxin exposure.
Obtain IV access, continuous ECG for electrolyte risk and accurate urine measurement.
Review all medicines immediately and withhold or dose-adjust nephrotoxic/renally cleared drugs under senior/pharmacy guidance.

ABCDE assessment

Step	Assess	Actions
A – Airway	Consciousness, uraemic vomiting, aspiration and seizures.	Position, suction and airway support when protective reflexes fail.
B – Breathing	Crackles, oxygenation, pulmonary oedema, Kussmaul breathing and acidosis.	Oxygen for hypoxaemia, ventilatory support and urgent fluid/renal review.
C – Circulation	BP, pulse, perfusion, dehydration, oedema, JVP and bleeding.	Careful fluid challenge if hypovolaemic; avoid overload and treat shock source.
D – Disability	Glucose, confusion, asterixis, seizures, headache and uraemic encephalopathy.	Check glucose/electrolytes; call renal/critical care for neurological deterioration.
E – Exposure	Rash, vasculitis, oedema, bruising, flank pain, catheter and abdominal/bladder findings.	Look for cause, prevent pressure injury and preserve dignity.

History and examination

Baseline creatinine/eGFR, previous CKD, dialysis access, transplant and renal specialist contact.
Fluid intake/losses, diarrhoea, vomiting, bleeding, fever, sepsis, burns, surgery, trauma and heart failure.
Urine volume, colour, froth, blood, pain, hesitancy, retention, stones and catheter history.
All medicines, over-the-counter NSAIDs, herbal products, contrast, antibiotics and recent dose changes.
Pregnancy/postpartum status, autoimmune symptoms, rash, joint pain, cough/haemoptysis and family renal disease.
Examine volume status, lungs, heart, abdomen, bladder, skin, joints, oedema, rash, pupils and mental status.

Investigations

Test	Purpose	Clinical action
Urea, creatinine and eGFR	Confirm and stage kidney deterioration.	Compare with baseline and trend daily or more often when unstable.
Electrolytes, bicarbonate, calcium, phosphate and magnesium	Detect hyperkalaemia, acidosis and mineral abnormalities.	ECG and immediate treatment for dangerous potassium/acid-base changes.
Urinalysis and microscopy	Look for blood, protein, casts, infection and specific gravity.	Glomerular findings need renal referral; culture suspected infection.
FBC, CRP, cultures and lactate	Find sepsis, anaemia, inflammation and hypoperfusion.	Sepsis treatment should not be delayed; adjust antibiotic doses for renal function.
Ultrasound urinary tract	Identify hydronephrosis, obstruction, kidney size and bladder retention.	Urgent urology review for infected obstruction or bilateral obstruction.
CK, blood film, autoimmune/serology tests	Investigate rhabdomyolysis, haemolysis, vasculitis, GN or systemic disease.	Specialist-directed; do not delay management of hyperkalaemia or shock.

Fluid and haemodynamic management

Determine whether the patient is hypovolaemic, euvolaemic or fluid overloaded using history, perfusion, lungs, JVP, oedema, weight and response to a small test bolus.
If hypovolaemic, give appropriate isotonic fluid and reassess BP, pulse, capillary refill, lungs and urine output after each bolus.
If septic, treat infection and perfusion promptly while avoiding both under-resuscitation and pulmonary oedema.
If fluid overloaded, restrict further fluid according to prescription, sit upright, provide oxygen/ventilatory support and involve renal/critical care.
Loop diuretics may treat symptomatic fluid overload but do not cure intrinsic AKI or replace dialysis when emergency indications persist.
Maintain accurate input/output, daily weight and prescribed fluid allowance.

Hyperkalaemia and acidosis

Obtain an urgent ECG and repeat potassium to exclude haemolysis, but treat life-threatening ECG changes immediately.
Call senior/renal/critical-care support. Stabilise the myocardium, shift potassium intracellularly and remove potassium according to the local hyperkalaemia protocol.
Stop potassium-containing fluids, potassium supplements, ACE inhibitors/ARBs, potassium-sparing diuretics and other contributors under prescriber guidance.
Monitor glucose, ECG and repeat potassium because rebound hyperkalaemia is possible.
Severe refractory hyperkalaemia, severe metabolic acidosis or arrhythmia may require urgent renal replacement therapy.

Obstruction and nephrotoxins

Check catheter patency, bladder volume and ultrasound when output falls unexpectedly.
Urgently refer infected obstruction, anuria, bilateral obstruction or obstruction in a solitary kidney to urology.
Stop or adjust nephrotoxic medicines and renally cleared drugs with a pharmacist/renal clinician.
Do not delay emergency contrast imaging when it is essential; assess risk, hydrate appropriately and avoid repeated unnecessary contrast.
Ask about traditional/herbal remedies and unknown tablets, which may be important causes in the local setting.

Indications for renal replacement therapy

Dialysis or continuous renal replacement therapy is considered when complications cannot be controlled medically. Use the clinical picture, trends and specialist decision rather than a creatinine number alone.

Refractory Acidosis causing instability.
Dangerous Electrolyte abnormality, especially persistent hyperkalaemia.
Dialysable Intoxication when the toxin and clinical criteria require it.
Fluid Overload causing pulmonary oedema despite medical treatment.
Uraemic complications such as encephalopathy, pericarditis, bleeding or severe symptoms.
Use the AEIOU principle, but remember that access, haemodynamics, resources and patient goals determine the modality.

Nursing interventions and monitoring

Measure urine output accurately, including catheter hourly output when unstable; document anuria/oliguria promptly.
Maintain fluid-balance chart, daily weight, oedema assessment, lung auscultation and prescribed fluid restriction.
Repeat BP, pulse, respiratory rate, SpO₂, ECG, mental state, potassium, bicarbonate and creatinine at the required frequency.
Use aseptic catheter care and avoid unnecessary urinary catheterisation.
Check every medicine for renal dose adjustment, nephrotoxicity and potassium effect.
Protect skin, maintain nutrition, manage pruritus/uraemic symptoms and prepare the patient for dialysis access/procedure.
Escalate falling urine output, arrhythmia, breathlessness, chest pain, confusion, seizure or bleeding immediately.

Special populations

Pregnancy: consider pre-eclampsia, haemorrhage, sepsis and thrombotic microangiopathy; involve obstetrics and renal services early.
Children: assess weight-based fluid needs carefully, congenital urinary disease and dehydration; avoid adult assumptions.
Older adults: creatinine may appear modest despite low renal reserve; use baseline trend and clinical status.
Heart failure: fluid resuscitation is high-risk; use small reassessed boluses, ultrasound/echo and critical-care input.
Sepsis: AKI may be an early marker of organ dysfunction; antibiotics and source control must be timely.

Complications

Complication	Clues	Response
Hyperkalaemia	Weakness, paresthesia, peaked T waves, broad QRS or arrhythmia.	ECG, immediate hyperkalaemia protocol and renal/critical-care review.
Pulmonary oedema	Dyspnoea, orthopnoea, crackles, hypoxia and rapid weight gain.	Upright position, oxygen/ventilation, fluid restriction, diuretic/dialysis review.
Metabolic acidosis	Kussmaul breathing, confusion, hypotension and low bicarbonate.	Blood gas, treat cause and consider renal replacement if refractory.
Uraemic encephalopathy/pericarditis	Confusion, asterixis, seizures, chest pain or friction rub.	Urgent renal/critical-care review and dialysis assessment.
Bleeding/infection	Bruising, GI bleeding, fever, catheter infection or sepsis.	Source control, cultures, antibiotics and specialist management.

Prevention, discharge and follow-up

Drink appropriately during illness, seek early help for vomiting/diarrhoea and avoid unsupervised NSAIDs or herbal medicines.
Tell every healthcare provider about previous AKI, CKD, allergies and current medicines.
Use sick-day medication advice only under a clinician’s written plan; do not stop essential medicines without guidance.
Repeat creatinine/electrolytes after discharge and arrange renal review for severe, recurrent, unexplained or incomplete recovery.
Teach red flags: reduced urine, swelling, breathlessness, weakness/palpitations, persistent vomiting, confusion or chest pain.

Clinical scenarios

Scenario 1 – Septic AKI: A patient with pneumonia is hypotensive and passes very little urine. Start ABCDE/sepsis care, obtain cultures, give carefully reassessed fluids, antibiotics and monitor lactate/urine output; involve critical care early.

Scenario 2 – Hyperkalaemia: A dialysis patient has weakness and a broad QRS. Attach ECG, call for help, treat life-threatening potassium toxicity immediately under protocol and prepare urgent renal replacement therapy.

Scenario 3 – Obstruction: An older man has anuria, suprapubic discomfort and a palpable bladder. Check catheter/bladder, decompress under local guidance, ultrasound for obstruction and arrange urgent urology review.

Common errors to avoid

Assuming AKI is present only when the patient reports pain or reduced urine.
Giving repeated large fluid boluses without checking lungs and perfusion.
Ignoring medicines, herbal products and contrast exposure.
Waiting for laboratory confirmation before treating ECG-proven hyperkalaemia.
Using diuretics to “fix” intrinsic AKI without addressing overload or dialysis indications.
Failing to investigate obstruction or to record accurate urine output.
Discharging without repeat renal tests, medication review and safety-netting.

AKI CARE: A – Assess volume and ABCDE; K – Keep ECG/glucose/electrolytes monitored; I – Identify cause and nephrotoxins; C – Correct shock, potassium and acidosis; A – Assess obstruction; R – Renal replacement when indicated; E – Educate and follow up.

Revision questions

Differentiate pre-renal, intrinsic and post-renal AKI with examples.
What clinical findings suggest fluid overload rather than dehydration?
List the immediate actions for ECG changes caused by hyperkalaemia.
What does the AEIOU dialysis mnemonic represent?
Why is urine output trend important even before creatinine returns?
Which medicines and exposures can worsen AKI?
Write a nursing monitoring plan for a critically ill patient with AKI.

Key takeaways

AKI can be silent, reversible and life-threatening.
Assess perfusion and volume carefully; treat sepsis, obstruction and nephrotoxins promptly.
Hyperkalaemia, acidosis, pulmonary oedema and uraemic complications need urgent escalation.
Accurate urine output, medication review, ECG and electrolyte trends guide safe care.
Dialysis decisions are clinical and specialist-led, not based on creatinine alone.