Metabolic Acidosis

Also known as: Acidaemia

Metabolic acidosis is a primary reduction in serum bicarbonate producing a fall in pH, compensated by an increase in alveolar ventilation that lowers PaCO₂.

The first and most useful step in assessment is calculating the anion gap, because it separates two entirely different differential diagnoses:

Raised anion gap acidosis results from added unmeasured acid, and is usefully remembered as GOLD MARK: Glycols (ethylene glycol, propylene glycol), Oxoproline (chronic paracetamol use), L-lactate, D-lactate, Methanol, Aspirin (salicylates), Renal failure, Ketoacidosis
Normal anion gap (hyperchloraemic) acidosis results from bicarbonate loss or impaired renal acid excretion, principally diarrhoea, renal tubular acidosis, and saline loading

Severity is driven less by the pH itself than by the underlying cause and the patient's ability to compensate; a patient with a pH of 7.2 from ketoacidosis and one with the same pH from cardiogenic shock have very different trajectories.

Blood gas confirming low pH and low bicarbonate, with a low PaCO₂ if respiratory compensation is intact
Assess compensation using Winter's formula: expected PaCO₂ ≈ (1.5 × HCO₃) + 8 ± 2. A PaCO₂ higher than predicted indicates a coexisting respiratory acidosis — often a tiring patient who can no longer sustain the work of breathing, which is an ominous finding. A PaCO₂ lower than predicted indicates a coexisting respiratory alkalosis
Anion gap: Na − (Cl + HCO₃), corrected for albumin
Delta ratio (change in anion gap divided by change in bicarbonate) identifies mixed disorders: a ratio below 1 suggests a coexisting normal anion gap acidosis, and above 2 a coexisting metabolic alkalosis
Directed investigations by suspected cause: lactate, glucose and ketones, renal function, salicylate and paracetamol levels, osmolar gap if toxic alcohol ingestion is possible, creatine kinase, and urinary anion gap if the gap is normal
Review the drug and fluid chart, including metformin, and the volume of saline given
In a normal anion gap acidosis, proceed as in the hyperchloraemic acidosis entry

Treat the underlying cause, which is almost always the definitive intervention: insulin and fluid for ketoacidosis, restoration of perfusion for lactic acidosis, antidote and dialysis for toxic alcohols, dialysis for uraemic acidosis, and rehydration for diarrhoeal losses
Bicarbonate is not routinely given, and its role remains genuinely contested. It is generally reserved for severe acidaemia (pH below approximately 7.1), for normal anion gap acidosis where bicarbonate has genuinely been lost, and for specific indications such as hyperkalaemia with acidosis, salicylate poisoning (where alkalinisation is therapeutic in its own right), and tricyclic antidepressant toxicity
The arguments against routine bicarbonate are substantive: it generates CO₂ which can worsen intracellular acidosis if ventilation is fixed, causes hypokalaemia and hypocalcaemia, produces sodium and volume loading, and shifts the oxygen dissociation curve. In diabetic ketoacidosis and lactic acidosis specifically, it has not been shown to improve outcomes
Support ventilation where respiratory compensation is failing. A rising or normalising PaCO₂ in a severely acidotic patient signals exhaustion and impending respiratory arrest, and is an indication for urgent critical care review rather than reassurance
Correct potassium, anticipating that it falls as acidosis is corrected and potassium shifts back into cells — this is the same dynamic seen in diabetic ketoacidosis management
Monitor gas, electrolytes and lactate serially to confirm the trajectory rather than relying on a single set

Referral: critical care for severe acidosis, haemodynamic instability, or failing compensation; nephrology for dialysis; toxicology for suspected poisoning.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Indications for Dialysis

Also known as: Renal replacement therapy

Dialysis is a renal replacement therapy used to remove waste products, correct electrolyte and acid base derangement, and manage fluid balance when native kidney function is insufficient to do so, whether in the context of acute kidney injury or end stage chronic kidney disease.

The two principal modalities are hemodialysis, in which blood is circulated through an external filter against a dialysate fluid across a semipermeable membrane, typically performed several times weekly in a dialysis unit or, in selected patients, at home, and peritoneal dialysis, in which the patient's own peritoneal membrane serves as the filtering surface, with dialysate instilled into and drained from the peritoneal cavity, typically performed daily at home either manually or via an automated overnight cycler.

The indications for urgent dialysis in acute kidney injury are commonly recalled using the mnemonic AEIOU, reflecting the specific, time critical complications that dialysis is used to correct when they fail to respond to medical management.

Acidosis, specifically severe metabolic acidosis that is refractory to medical correction, is an indication, since uncorrected severe acidosis carries significant cardiovascular and metabolic risk.

Electrolyte abnormality, most commonly severe or refractory hyperkalemia not adequately controlled by medical measures (calcium, insulin and glucose, salbutamol, potassium binders), is one of the most common acute indications given the immediate arrhythmic risk of significant hyperkalemia.

Intoxication with a dialyzable substance, such as certain overdoses (for example lithium, salicylates, or methanol and ethylene glycol among others), is an indication where dialysis can meaningfully accelerate toxin clearance.

Overload of fluid, causing pulmonary edema refractory to diuretic therapy, particularly in an oliguric or anuric patient where diuretics have limited further effect, is an indication.

Uremia, specifically the clinical complications of uremia rather than a biochemical urea level in isolation, including uremic encephalopathy, uremic pericarditis, and significant uremic bleeding tendency, is an indication, since these represent the clinical manifestations that dialysis is specifically intended to reverse.

Dialysis initiation in progressive chronic kidney disease is generally guided by a combination of eGFR trajectory and the development of specific symptoms or complications, rather than by an eGFR threshold in isolation, since the timing of initiation based on symptoms rather than a fixed number has been shown not to disadvantage patients and avoids unnecessarily early initiation.

Indications include the same AEIOU categories as above when they occur in the context of progressive, irreversible chronic kidney disease rather than resolving acute injury, alongside the development of significant uremic symptoms (nausea, anorexia, pruritus, cognitive change), malnutrition attributable to advanced renal failure, and an eGFR that has fallen to a very low level (generally in the range of 5 to 10 mL per minute per 1.73 m squared) even in the relative absence of overt symptoms, given the recognized risks of delaying initiation too long in this setting.

Planning for chronic dialysis, including the choice of modality and, for hemodialysis, the creation of vascular access such as an arteriovenous fistula well in advance of anticipated need, should ideally begin once a patient's chronic kidney disease trajectory suggests dialysis is likely to be required within the coming months to a year or so, since late referral and unplanned dialysis initiation, often via an emergency central venous catheter, carries worse outcomes than planned initiation with established access.

The choice between hemodialysis and peritoneal dialysis is guided by a combination of patient preference, lifestyle, comorbidity, and specific contraindications. Peritoneal dialysis is generally contraindicated or relatively unsuitable in patients with extensive prior abdominal surgery, significant abdominal wall hernia, or an inability to manage the technique either independently or with adequate support. Hemodialysis requires adequate vascular access and the ability to attend a dialysis unit regularly, unless home hemodialysis is being pursued.

Renal transplantation remains the optimal form of renal replacement therapy where feasible, offering superior long term survival and quality of life compared with either dialysis modality, and should be actively considered and discussed with suitable candidates, ideally well before dialysis becomes necessary, to allow for pre-emptive transplantation where a suitable donor is available.

Referral: nephrology for planning of renal replacement therapy in progressive chronic kidney disease, ideally well in advance of anticipated need; urgent nephrology involvement for any acute indication for dialysis in the context of acute kidney injury.

Metabolic Acidosis

Overview

Diagnosis

Management

Overview

Indications in Acute Kidney Injury

Indications in Chronic Kidney Disease

Choice of Modality