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Blood gas case 1: renal failure and type 1 diabetes

Blood gas interpretation svhm icu

Peer reviewed by Dr Steven Musca and Dr Patricia Hurune

Case details

55 year old male with known ESRF presented to hospital with shortness of breath after missing haemodialysis (HDx).

PMHx: CKD-5D (HDx 3x/wk via AV fistula), T1DM, HTN

VBG on presentation:

VBG Parameter Patient Value Normal Range
pH 7.13* 7.31 – 7.41
pCO2 43mmHg 40 – 50
pO2 61mmHg* N/A
HCO3 14mmol/L* 22 – 26
Base Excess -14.4mmol/L* -2 to +2
Hb 101g/L* 120 – 160
Na 122mmol/L* 135 – 145
K 7.7mmol/L* 3.5 – 4.5
Cl 87mmol/L* 98 – 106
Glucose >60.0mmol/L* 3.9 – 5.8
Lactate 4.4mmol/L* < 1.6

Interpretation of blood gases

A common question for the CICM Second Part Examination is interpretation of a blood gas, with a request to comment on the specific abnormalities of the blood gas. Having a structure will ensure you don’t miss any important details in the exam or on your next ward round. In this blog post I’ll demonstrate a structure I use to help interpret blood gases.

My structure starts with the assumption that there is only one normal arterial blood gas (note: VBG values vary slightly):

pH = 7.4
pCO2 = 40mmHg
HCO3 = 24mmol/L

Any deviation from this is then described using the various rules for acute/chronic respiratory/metabolic acidosis/alkalosis. (See references 1 and 2).

NB: for this blog post we will be looking at VBGs only, and we will omit my usual first step of assessing adequacy of oxygenation and determination of A-a gradient (to be covered in a future post!)

Question 1. Describe the acid-base abnormalities on the above blood gas.

1a. Is there an acidaemia or alkalaemia?

Click to see answer

There is an acidaemia (pH < 7.31 on VBG).

1b. Is the acidaemia explained by a respiratory or metabolic abnormality?

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In this example the pCO2 is in the normal range for a VBG, which doesn’t explain the acidaemia. However, the HCO3 is < 22, which fits with a metabolic acidosis contributing to the acidaemia.

1c. Assess for compensation using ABG interpretation rules

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The expected pCO2 would be 1.5x[HCO3] + 8 = 29; therefore, there is likely a respiratory acidosis, or inadequate compensation; however interpretation must be cautious from a VBG (rule applies for paCO2).

1d. For the metabolic acidosis, determine if the anion gap (AG) is high or normal

Click to see answer

AG = Na – (Cl + HCO3)
Normal value = 12
This is a high anion-gap metabolic acidosis (HAGMA), with an AG of 122 – (87+14) = 21

1e. Determine the delta gap or delta ratio

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This is done to determine if the acidosis is entirely due to the extra anions in the AG, or if there is also another cause contributing to the acidosis (i.e. a co-existing normal anion-gap metabolic acidosis – NAGMA)

Delta gap = (change in AG) – (change in HCO3)
where normal AG = 12, and normal HCO3 = 24
Delta gap < -6 implies there is a mixed HAGMA and NAGMA
Delta gap -6 to 6 implies there is only a HAGMA, with no co-existing NAGMA
Delta gap >6 implies there is a mixed HAGMA and a metabolic alkalosis

The delta gap is (21-12) – (24-14) = 9-10 = -1 suggesting only HAGMA

The delta ratio uses the same information, but is a ratio comparison

Delta ratio = (change in AG) / (change in HCO3)
<0.4 = NAGMA
0.4 – 0.8 = mixed HAGMA and NAGMA
0.8 – 2 = pure HAGMA
>2 = mixed HAGMA and a metabolic alkalosis

The delta ratio is 9/10 = 0.9 –> suggests pure HAGMA (see reference 3)

1f. Note other relevant features

Click to see answer

There is a lactic acidosis, with a raised lactate of 4.4.

NB: although a raised lactate is one of the causes of a high anion-gap, the lactate of 4.4 mmol/L does not explain the whole increase in the AG from 12 (normal) to 21. There are 9mmol/L of “extra anions” so something else must also be contributing.

There is also anaemia, hyponatremia, a significant hyperkalaemia and hyperglycaemia.

This question is a good example of how to work through an approach to metabolic acidosis on a blood gas.

Question 2. What are the general causes of a HAGMA?

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A common mnemonic for HAGMA is “Left Total Knee Replacement” or LTKR

LTKR – Lactic acidosis, Toxins, Ketones and Renal failure

As you can see – all of the above could be contributing to this case.

There are many potential causes of a lactic acidosis, and several possible toxins include ethylene glycol, methanol and pyroglutamic acidosis.

Question 3. What are some of the specific contributors in this case?

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Lactic acidosis – shock/sepsis related?
Ketones – DKA
Renal failure – known ESRF

Question 4. The formal EUC comes back as below. Please comment on the abnormalities with a possible cause for each.

Parameter Patient Value Normal Range
Na 121 mmol/L* 135 – 145
K 8.3 mmol/L* 3.5 – 2.0
Cl 82 mmol/L* 98 – 109
Urea 22.9 mmol/L* 2.1 – 7.1
Creatinine 465 umol/L* 49 – 90
Bilirubin 14 umol/L <20
ALT 36 U/L 35 – 50
ALP 95 U/L* <38
GGT 168 U/L* 40 – 100
Glucose 74.0 mmol/L* 3.0 – 7.7

Ketones: 5 mmol/L (on bedside fingerprick)

Click to see answer

Hyponatraemia – possibly hypervolaemic due to missed haemodialysis (HDx), pseudohyponatraemia due to hyperglycemia
Hyperkalaemia, hyperphosphataemia – in setting of missed HDx
Renal impairment – known ESRF
Mildly deranged LFTs with obstructive pattern – ?possible trigger for DKA, or just part of illness
Hyperglycaemia, ketosis – T1DM with poor control  DKA

ECG:


Question 5. The following ECG was taken. Comment on the abnormalities seen

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HR approximately 60, sinus rhythm
Borderline right axis deviation
Increased PR interval (>0.2ms)
Mildly increased QRS duration (>0.12ms)
Widespread peaked T-waves, consistent with hyperkalaemia

Question 6. What would be your immediate management in this scenario?

Click to see answer

Progress:

Received IV Ca2+ (membrane stabilisation), salbutamol, dextrose-insulin, NaHCO3 and antibiotics in ED as well as some 0.9% saline volume resuscitation. Transferred to ICU for urgent HDx and a DKA insulin protocol which saw correction of the biochemical and ECG abnormalities. Discharged to ward 2 days later for ongoing titration of subcutaneous insulin.

Great work!

Disclaimer: this is a fictional case for educational purposes that may contain de-identified patient data.

References:

1) Brandis, K. Acid-base physiology, http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php, last accessed 15th August 2020

2) Foot, C. Steel, L. et al (2012) Examination Intensive Care Medicine, second edition, Elsevier Australia, pg 176

3) Nickson, C. Delta Ratio, Life in the Fast Lane, https://litfl.com/delta-ratio/, last accessed 15th August 2020

4) Yartsev, A. Delta gap and delta ratio, Deranged Physiology, https://derangedphysiology.com/main/cicm-primary-exam/required-reading/acid-base-physiology/Chapter%20705/delta-gap-and-delta-ratio, last accessed 20th August 2020

2 thoughts on “Blood gas case 1: renal failure and type 1 diabetes

  1. In question 4, it may be that the extremely high glucose is contributing to a pseudohyponatraemia. The corrected sodium appears to be either normal or mildly elevated depending on the correction used.

    1. Hey Nathaniel,
      Great pick-up, you’re absolutely right! Thanks for the comment.
      For those interested in more, you can calculate the corrected sodium with freely available online calculators.
      Could be a good area for a future blog post…

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