A 19 year old pregnant insulin dependent diabetic patient was admitted with a history of polyuria
and thirst. She now felt ill and presented to hospital. There was a history of poor compliance with
She was afebrile. Chest was clear. Circulation was adequate. Perioral herpes was
present. Urinalysis: 2+ ketones, 4+ glucose. Biochemistry on admission: Na+ 136, K+ 4.8, Cl- 101,
bicarbonate 10, glucose 19.0, urea 8.1 and creatinine 0.09 (all biochem results in mmol/l). Arterial blood gases were collected on arrival.
First: Initial clinical assessment
The diagnosis is obvious on history: the patient has a severe diabetic ketoacidosis. With such an obvious diagnosis, why bother with the systematic approach?
The systematic approach has several advantages:-
The first step incorporates all this clinical expectation (i.e. in "the initial clinical assessment" stage) so there
is nothing lost. The obvious diagnosis becomes the hypothesis which is tested in the rest of the analysis. In this case, the hypothesis is
"This patient has a diabetic ketoacidosis". Now we have to confirm the diagnosis
The approach will generally detect the presence of other concurrent acid-base disorders that are not obvious
It provides a framework to synthetize the acid-base results with the overall clinical situation
(i.e. 'the clinical diagnosis' step)
This patient has diabetic ketoacidosis(DKA), but such patients may have other acid-base disaorders present, such as:
a co-existent lactic acidosis (related to poor tissue perfusion)
a hyperchloraemic metabolic acidosis (due replacement of keto-anions lost in the urine with
chloride by the kidney and as a result of saline resuscitation fluids)
a respiratory acid-base disorder is possible if (for example) pulmonary infection is the
cause, or if there is a decreased level of consciousness
Second: The acid-base diagnosis
pH: The acidaemia indicates the presence of an acidosis
Pattern: The combination of a low bicarbonate and a low pCO2 is typical of a metabolic acidosis
Clues: The hyperglycaemia, glycosuria and ketonuria indicate the presence of a diabetic ketoacidosis.
The anion gap is elevated (at 25) supporting a diagnosis of a high anion gap disorder.
There is no evidence of renal failure. The delta ratio is (25-12)/(24-7) = 0.76 and
the chloride level is normal as is [Na+], so no evidence of a concurrent hyperchloraemic acidosis.
Compensation: The appropriate rule to assess compensation for a metabolic acidosis
is (rule 5). The expected pCO2 is (1.5 x 7.1 + 8) = 18.5mmHg.
The actual pCO2 is only 2 mmHg different so there is no evidence of a co-existing respiratory acid-base disorder.
Sufficient time (12-24 hours) has passed so compensation would be expected to have reached its maximum value. (Maximal compensation is insufficient to return the pH to normal)
Formulation: A severe metabolic acidosis (diabetic ketoacidosis) is present. There is
no evidence of any other acid-base disorder. The delta ratio is not low enough nor the chloride
level high enough to indicate a definite hyperchloraemic acidosis, but this commonly develops
during treatment. A lactic acidosis component cannot be totally excluded as no lactate result
has been recorded but the fact that the urine test for ketones was reactive argues against a
major component of lactic acidosis
Confirmation: A lactate level would be useful.
in such cases
Finally: the Clinical Diagnosis
Diabetic ketoacidosis due to poor compliance with diabetic treatment.
This case history is of a patient with a high anion gap metabolic acidosis. The overview of
causes in the table below is what a clinician should have a mental picture of as they
approach the differential diagnosis of a high anion gap acidosis.
Diabetic ketoacidosis is the commonest severe acid-base disorder that presents to hospital
so you should be particularly familiar with this diagnosis.
Overview of Classification of Causes of a Metabolic Acidosis
Principle: Metabolic Acidosis is classified into 2 major groups based on whether the Anion Gap is normal or
elevated (see Section 5.2.2)
First Group: High anion gap metabolic acidosis (HAGMA)
Low pH => significant acidaemia => therefore an underlying acidosis is present
Both pCO2 and HCO3 are low => therefore a metabolic acidosis is present
The Anion Gap is elevated, therefore a high anion gap metabolic acidosis (HAGMA) is present
So the diagnosis so far is that a HAGMA is present. Now determine the cause among the following 4 groups:
Ketoacidosis - Diagnosis is supported by history, hyperglycaemia, glycosuria & ketouria
Lactic acidosis - Often a diagnosis of exclusion but should be diagnosed based on a lactate
level. Then consider whether the cause is poor perfusion (type A) or not (type B)
Acidosis due to renal failure - Diagnosis not supported as no azotaemia
Acidosis due to toxins - This is often a diagnosis based on history and/or CNS signs
In this case, the patient recovered with management but compliance with diabetic therapy continued to be
poor. An intrauterine foetal death occurred four months after this admission.
This patient had had several previous admissions with diabetic ketoacidosis.
Results on presentation five months prior to the admission discussed in the example were:
Other biochemistry: Na 140, K 4.3, Cl 111, glucose 24.8, urea 4.6 mmol/l. The delta ratio is about 0.68 indicating concurrent HAGMA and NAGMA (as in range 0.4-0.8)
1. The major diagnosis can often be made on initial clinical assessment, but a systematic analysis is needed to detect concurrent acid-base disorders
2. Metabolic acidosis is classified into 2 groups depending on the Anion Gap
3. A high anion gap alerts to the presence of an underlying HAGMA