Deployed Management of Renal Failure

Objectives

To provide a standardised approach to the assessment and management of acute kidney injury (AKI) in the deployed setting. 
To support early recognition and timely intervention for those requiring renal replacement therapy (RRT).

Scope

This guidance applies to adult patients with suspected or confirmed AKI, within Role 1, 2 and 3 facilities and during prolonged casualty care. 

Audience

Deployed clinicians providing ICU-level care in austere settings.

Initial Assessment & Management

The initial assessment and management of severe acute kidney injury should follow a structured approach, focusing on timely identification of those at risk of requiring renal replacement therapy (RRT), and the prompt initiation of temporising interventions.

Recognition of severe acute kidney injury

Risk factors in the deployed setting

  • Trauma, major haemorrhage, shock
  • Rhabdomyolysis + crush injury
  • Prolonged tourniquet time
  • Sepsis
  • Dehydration + heat injury

Clinical features

  • Reduced or absent urine output
  • Altered mental status
  • Volume overload
  • Electrolyte and acid-base abnormalities (hyperkalaemia/acidosis)
  • Raised creatinine (if available)

Early optimisation of renal perfusion

Volume status should be assessed and hypovolaemia corrected promptly, balancing the need for renal perfusion against the risk of fluid overload.

Endpoints of resuscitation may include:

  • improvement in haemodynamic parameters
  • restoration of urine output
  • improving mental status
  • normalisation of lactate
In active haemorrhage, blood products should be used in preference to crystalloids in accordance with DCR principles.
Without active haemorrhage, balanced crystalloid solutions (Plasmalyte 148 or Hartmann’s/Compound Sodium Lactate) should be used for volume expansion. Colloids, and large volumes of 0.9% NaCl should be avoided.
Vasopressors should be used after volume resuscitation to maintain a mean arterial pressure over 65mmHg, in order to avoid fluid overload in established renal injury. Standard protocols can be used, with noradrenaline as the first line agent. 

Early recognition and treatment of life-threatening complications

Life-threatening complications of hyperkalaemia and/or severe metabolic acidosis must be actively sought out and aggressively treated. Management algorithms for temporising measures can be found within the subsections below.

If these complications arise, RRT may be required so discuss early with the Aeromedical Evacuation Control Centre (AECC). Details are provided in AP3394. 

Fluid balance monitoring

Insert a urinary catheter, with strict input/output monitoring hourly. Oliguria is defined as < 0.5ml/kg/hr in adults. Consider insensible losses in heat injury, exertional rhabdomyolysis, or in patients following damage control surgery.

Drug considerations 

Stop and avoid further nephrotoxic drugs. Diuretics should not be used to promote urine output. Ensure drug dosing is adjusted for renal impairment; in particular opioids and antibiotics will often need dose reduction.

Advanced Assessment & Management

Determining Aetiology 

Early identification of the underlying cause is essential to guide treatment and inform evacuation decisions. Many will have both pre-renal and intrinsic injury in an operational setting. 


Pre-renal
Causes: hypovolaemia, shock, high intra-abdominal pressures Clues: haemodynamic instability, concentrated urine, improved urine output with fluid resuscitation Priorities: early volume resuscitation, avoidance of diuretics
Intrinsic renal
Causes: acute tubular necrosis (shock/sepsis/rhabdomyolysis/crush), nephrotoxins, glomerulonephritisClues: oliguria despite fluids, rising Creatinine, coca-cola urine, rising CK, hyperkalaemia and acidosisPriorities: stop nephrotoxins, conservative fluids only after euvolaemia achieved, early RRT planning 
Post-renal 
Causes: catheter blockage, traumatic pelvic/urethral injury, external compression from binders/packing Clues: anuria or fluctuating urine output, suprapubic fullness, residual on bladder ultrasound. Priorities: catheterise and check patency, surgical consultation if obstruction suspected

Investigations

Point of care testing (e.g i-STAT) should be used to rapidly assess electrolyte and acid-base disturbances when conventional laboratory support is unavailable. Urinalysis may be useful when all other tests are unavailable. All investigations should be used to monitor trends, not interpreted in isolation.  

Recommended point of care tests: potassium, sodium, bicarbonate, ABG, lactate


Laboratory
Creatinine (rise can be delayed in acute injury) 
Urea/Blood urea nitrogen (BUN) 
Creatine kinase (if suspect rhabdomyolysis, crush, heat injury) 
 
Urinalysis 
Blood: indicative of trauma to the urinary tract, rhabdomyolysis, crush or heat injury. 
Protein: a non-specific marker of glomerular injury and severe AKI 
Ketones: raised in hypovolaemia, heat illness and metabolic acidosis 
Glucose: raised in trauma, sepsis, tubular injury. 
 

Renal replacement therapy (RRT) capability

Renal replacement therapy (NxStage 1) is a Defence capability held by the Critical Care Air Support Team (CCAST) at Tactical Medical Wing (TMW) in RAF Brize Norton.

The RRT module is held at R0 (6 hours NTM) and activation is coordinated by AECC. Details are in AP3394.

Activation will provide the RRT module, and 2 RRT flight nurses. RRT will typically be completed on the ground, prior to aeromedical evacuation, as per the CCAST SOP.

Indications: hyperkalaemia refractory to medical therapy, refractory fluid overload causing respiratory compromise, symptomatic uraemia, worsening metabolic acidosis despite resuscitation, drug overdose with dialysable toxins

Prolonged Casualty Care

Incidence of AKI

While severe AKI on operations is rare, the incidence and severity is likely to increase in conflict with prolonged evacuation time, and limited forward resuscitation capabilities.

Monitoring 

Regular monitoring and close attention to fluid balance, acid-base and electrolytes is essential during periods of prolonged field care. Clinical assessment and point of care investigations are the mainstay.

Treatment considerations

In prolonged casualty care, sodium zirconium cyclosilicate (Lokelma) may be useful for oliguric patients with repeated hyperkalaemia despite temporising measures, prior to RRT initiation. A protocol for use is found within the Hyperkalaemia submenu below.

Lokelma can reduce the frequency of temporising IV therapies, therefore reducing depletion of deployed consumables.

RRT Considerations 

If RRT is activated and skillset allows, vascular access with a 12-14 Fr dialysis catheter can be gained. 

  Location Length of catheter Comments
1st line Right internal jugular vein 15cm  
2nd line Femoral vein 20-25cm  
3rd line Left internal jugular vein 20cm  
4th line Subclavian vein 15cm Avoid if possible due to venous stenosis risk.

 

Management of hyperkalaemia

Hyperkalaemia is a time-critical, life-threatening complication of AKI with risk of malignant dysrhythmia at K⁺ >6.5 mmol/L.

Approach

ABCDE 
12-lead ECG and continuous cardiac monitoring

Look for ECG changes in hyperkalaemia 
Peaked T waves 
Broad QRS 
Flattened or absent P waves 
Bradycardia 
Sine-wave pattern or ventricular tachycardia 

Treatment Algorithm

Mild (K⁺ 5.5–5.9 mmol/L):

Monitor potassium and ECG, treat reversible cause

Moderate (K⁺ 6.0–6.4 mmol/L):

If ECG changes present: give 30mls of 10% Calcium gluconate IV over 10 minutes via large IV access or 10mls of Calcium chloride 10% over 5 minutes (CVC preferred) before any other therapy.

1. Give insulin–dextrose therapy: Actrapid 10 units IV in 25 g glucose over 15 minutes. 
25g glucose = 50mls 50% dextrose OR 125ml 20% dextrose OR 250mls 10% dextrose
If pre-treatment glucose <7 mmol/L, give 10% dextrose at 50 mL/hr for 5 hours 
Monitor blood glucose of all patients for 6 hours 
2. Give salbutamol :10–20 mg nebulised 
3. If available, give sodium zirconium cyclosilicate (Lokelma®) : 10 g PO (if GI tract functioning) 


Severe (K⁺ ≥6.5 mmol/L)Give calcium therapy immediately, regardless of ECG findings 

1. Follow full moderate-severity treatment algorithm.
2. Refer for RRT if refractory or recurrent hyperkalaemia, worsening AKI or life-threatening ECG changes.

 

 

Sodium Zirconium Cyclosilicate (Lokelma®)
Indicated in hyperkalaemia >6.0 mmol/L with functioning GI tract 
Bridging therapy after temporising measures and prior to RRT 
Not routinely carried in UK medical modules; may be available via local or partner-nation resources
Lokelma(®) Correction Phase 
10 g PO TDS (suspension in water) 
May be administered via nasogastric tube 
Lokelma(®) Maintenance Phase 
5 g PO OD 
Uptitrate to 10 g PO OD if required to maintain normal serum potassium

Metabolic Acidosis

Metabolic acidosis is an arterial blood pH < 7.35, with a plasma bicarbonate < 22mmol/L. Severe metabolic acidosis (pH < 7.2) may be life-threatening. 

Clinical Effects: reduced myocardial contractility, increased respiratory work, worsens hyperkalaemia
Management Priorities 

Reverse underlying cause and give 100% oxygen 
Optimise ventilation (increase respiratory rate if ventilated) 
Check serum potassium and treat hyperkalaemia
Give sodium bicarbonate therapy if severe acidosis, haemodynamic instability, or severe hyperkalaemia
Sodium bicarbonate therapy: 8.4%: 2 mL/kg via CVC only unless peri-arrest (max rate 1.5ml/kg/hr) OR 1.26%: 200–500 mL IV over 15–60 minutes. Monitor serum sodium and volume status 
Early referral for RRT if refractory acidosis 

Rhabdomyolysis

Rhabdomyolysis can directly cause AKI and requires early recognition and aggressive management. 

Suspect if
Significant muscle injury or prolonged ischaemia 
Severe muscle pain, swelling, or compartment syndrome 
Dark or coca-cola–coloured urine 
Unexplained hyperkalaemia or metabolic acidosis 
Laboratory Findings 
CK >5,000 IU/L (when associated with AKI) 
Rising creatinine 
Hyperkalaemia 
Hyperphosphataemia 
Hypocalcaemia 

Management Priorities Do not delay treatment while awaiting CK results. CK may be delayed or unavailable in the deployed setting.

Early aggressive IV fluids (balanced crystalloids) 
Target urine output >2–3 mL/kg/hr                                                                                                
Give sodium bicarbonate 1.26% IV to alkalinise the urine if adequate urine output and pH < 7.2
Avoid if oliguric or volume overloaded 
Aim urine pH >6.5 
Do not routinely treat hypocalcaemia unless symptomatic - risk of rebound hypercalcaemia
Anticipate and treat hyperkalaemia early
Urgent surgical review for fasciotomy or debridement of any limb injury
Refer for RRT if severe hyperkalaemia, severe metabolic acidosis, uraemia, or clinical deterioration

Toxicological causes of AKI

Toxicological AKI should be managed based on toxidrome and physiology, not confirmed diagnosis. 

Suspect if
Unexplained metabolic acidosis 
AKI out of proportion to shock 
High osmolar gap (if available) 
Unusual urine appearance or crystals 

Management Priorities 

Do not delay treatment awaiting toxicological confirmation

Airway protection 
Haemodynamic stabilisation 
Activated charcoal (early presentation, protected airway) 
Sodium bicarbonate for urinary alkalinisation in suspected salicylate poisoning 
Antidotes (if available and strongly suspected) 
Correct electrolyte abnormalities 
Avoid nephrotoxins 
Early referral for RRT if
Severe acidosis or hyperkalaemia   
Suspected ingestion of a dialysable toxin 
Dialysable Toxins (examples, not exhaustive)
Ethylene glycol 
Methanol 
Salicylates (aspirin) 
Lithium 
Valproate 
Metformin 

Last reviewed: 16/06/2026

Next review date: 16/06/2027

References

UK Kidney Association Clinical Practice Guidelines Treatment of Acute Hyperkalaemia in Adults. October 2023.

Joannidis M, Druml W, Forni LG, Groeneveld ABJ, Honore PM, Hoste E, Ostermann M, Oudemans-van Straaten HM, Schetz M. Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017 : Expert opinion of the Working Group on Prevention, AKI section, European Society of Intensive Care Medicine. Intensive Care Med. 2017 Jun;43(6):730-749. doi: 10.1007/s00134-017-4832-y. Epub 2017 Jun 2. PMID: 28577069; PMCID: PMC5487598.