Computer-based scenario

Biochemistry

How to read bloods?

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 Conflicts of interest

• None

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 Overview

• Part 1
– Structure of a biochemical case

– Approach to a difficult AB cases

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How is a case created and evaluated?

STRUCTURE OF A BIOCHEMICAL
CASE

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 CBS Biochemistry

• Less cases than in other CBSs (typically 8)

• All cases are real-life cases
• Arranged with increasing difficulty
– As per judgment of the author, not necessarily the
candidate.
• Time is a crucial issue
– Tests “pattern recognition”, rapid diagnosis
– If time is left, candidate is allowed to go back.

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 CBS slide

• Brief introduction to case (clinical context)

“28 year old alcoholic presents with 3 days of
nausea and vomiting. He looks unwell, HR 134/min,
but vital functions are stable”
• Laboratory picture in unified format
• Question (1-2 clear questions)
– Usually on diagnosis or immediate management

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 24 year old patient brought to emergency
Introductory vignette as title
department due to confusion.

Sodium 136 mmol/L Venous Blood Gas.

Potassium 7.2 mmol/L pH 6.870
Chloride Ions 111 mmol/L pO2 2.65 kPa (20 mmHg)
Ionized Calcium
Glucose 0.89 mmol/L pCO2 Blood gas
3.17 kPa (36 mmHg)
Anion Gap 27.8 mM HCO3- (st) 4.4 mmol/L
Hb Base Excess -28.7 mmol/L
Lactate 2.3 mM
Organ function
Glucose markers
23.7 mmol/L 427 mg/dL

Haemoglobin 16.1 g/dL (161 g/L)

What is the diagnosis?

URINE or QUESTION
What is the immediate management?

UrineOther, non-routine bloods

Ketones +++
Glucose +++

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 Expected Answers

• Diabetic ketoacidosis
• Intravenous crystalloids
• Intravenous insulin
• Consider bicarbonate if K+ not decreasing soon
• ECG and consider i.v. Ca2+

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 General features of cases

• Go straight to the point – answer question

• Points are given for the synthesis of information
or recognizing patterns. No points for
description of pathological values, e.g.
– “Hyperkalemia”
– “High hemoglobin due to dehydration”
– “Lactate 2.3 mM due to tissue hypoperfusion”
• You can should think aloud, but avoid
machinegun answers.

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Clinical context is crucial

THE VIGNETTE

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 Read the vignette!

• What diagnoses you may expect?

– REMOVED FROM DATABASE: 82 years old man
after CABG with multiple thrombotic episodes and
dropping platelets.
• HIT – dg. Possible from vignette alone
– 18 years old with vomiting and confusion
• Overdose = alcohol or illegal drugs?
• CNS infection?
• DKA?

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 Read the vignette!

– 65 year old patient with haemoptysis, no chest

pain or shortness of breath.
• Coagulation abnormality?
• Infections incl. TB Inflammatory markers?
• Lung tumour? ….SIADH? Low Na?
• Goodpasture?... Proteinuria? Urea, crea?
– Patient treated for preeclampsia.
• Mg2+?
• HELLP?
• Proteinuria?

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 Previous 24 hrs treated for pre-eclampsia. Transferred
to ICU with bradycardia 40 bpm and poor cough.

Sodium 135 mmol/L Arterial Blood Gas. 15 L/min O2 via face

mask
Potassium 3.8 mmol/L pH 7.310
Chloride 110 mmol/L pO2 36.3 kPa (274 mmHg)
Ionized Calcium 1.11 mmol/L pCO2 7.15 kPa (36 mmHg)
Phosphate 0.8mmol/L HCO3- (st) 25.5 mmol/L
Urea 16.6mmol/L (149 mg/dl) Base Excess +1.5mmol/L
Creatinine 220 umol/L (2.4 mg/dL) Lactate 0.9mmol/L
Glucose 10.0 mmol/L(180 mg/dl)
Haemoglobin 12.8 g/dL (128 g/L)
WBC 12.0 G/L What is your diagnosis?
PLT 348 G/L How do you confirm it?
Coagulation Normal

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 Expected Answer

• Hypermagnesaemia/measure Mg2+

• Support diagnosis, but no points for:

– Respiratory acidosis (?due to muscle weakness)
– AKI (? Due to pre-eclamsia)

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Algorithmic approach to a difficult acid-base cases

ADVANCED ACID-BASE FOR EDIC II

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 How to look at blood gas data

• Abnormality may not be instantly obvious

• Find your way how to find hidden complex
metabolic abnormalities, which are correcting
each other, resulting in normal acid base data.
– Frequent occurrence in CBS (and in clinical
practice)
– Exam authors like them.
• Sick people have sick values. If not, look again!

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 28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
functions are stable. Abdomen soft and non-tender

Sodium 132 mmol/L Arterial Blood Gas. 15 L/min O2 via

face mask
Potassium 4.6 mmol/L pH 7.432
Chloride 70 mmol/L pO2 28.3 kPa (212 mmHg)
Ionized Calcium 0.61 mmol/L pCO2 4.81 kPa (36 mmHg)
HCO3- (st) 24.3 mmol/L
BE -0.7 mmol/L
Glucose 8.0 144
mmol/L mg/dL
Haemoglobin 12 g/dL (120 g/L)
Describe acid-base disorder and give
possible causes.
Urine Ketones +
Glucose -

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 Classical Danish model

• Looks at bicarbonate buffer

• Based on Henderson-Hasselbalch equation
[HCO3-] Metabolic disorders
pH = 6.1 + log
α*pCO2 = acidosis
= alkalosis

Respiratory disorders
= alkalosis
= acidosis

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 Problem 1

• CO2 and HCO3- are not independent on each

other
CO2 + H2O  [H2CO3]  HCO3- + H+

– Consequence: acute CO2 retention causes instant

HCO3- elevation (i.e. before renal HCO3-
retention occurs)
• Solution:
– Concept of standard bicarb (Jorgensen&Astrup, 1957)
– Base Excess (P. Astrup, O. Sigaard Andersen, 1958)

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 HCO3- (actual)=
calculated by H-H
equation from pH
and pCO2

BE = mM of acid needed to
HCO3- (standard) = return pH to 7.40 under
corrected to pCO2=5.33 kPa
pCO2=5.33kPa BE (B)= blood (actual Hb)
BE (ect)=model of ecf (1/3 of
Hb)
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 Problem 1 solved

• HCO3- (actual)
– Influenced by pCO2 (H++HCO3- <-> CO2+H2O)

• HCO3- (standard) or Base Excess

– Adjusted to pCO2=5.3 kPa, i.e. shows net
metabolic component of disorder

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 Compensation

• Never complete in acute disorders

• Boston school = set of rules how to assess the

adequacy of compensation
– Only one is simple and useful: pCO2 in MAC
should be (HCO3act/5)+1kPa [±0.3 kPa]

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 What do you do?

• 21 yr girl with presumed DKA seen in emergency

room with HCO3-(act) = 7 mM
– Situation A: pH 7.09; pCO2 2.3 kPa
– Situation B: pH 7.32; pCO2 1.3 kPa
– Situation C: pH 6.92; pCO2 3.3 kPa
• Predicted pCO2 = (7/5)+1 = 2.3±0.3 kPa
– A: OK, medical HDU, treat DKA
– B: mixed MAC+RAL, investigate (e.g. salicylate? HCG?)
– C: ICU as impeding respiratory failure

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 Stage I – diagnosis of MAC

AG <16 mM=
Hyperchloridaemic MAC = Elevated AG (>16 mM)=
bicarbonate loss find circulating acid
•GI? •Lactate?
•Kidney? •Ketones?
•Too much chloride? •Retained inorganic
acids in AKI?
•Poison?

Other Other
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+≠- +=-

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 Thinking algorithm
(stage I – Medical Student)

• Identify the type of disorder (e.g. MAC)

– Bicarbonate (actual) or BE/standard bicarbonate
• Identify its cause – clinical context
– Calculate AG = (Na+K)-(Cl+HCO3-) [<16mmol/l]
• If elevated, find the acid
• If normal, find where is bicarbonate being lost from
• Assess the degree of compensation
– Eg. Boston rule to assess pCO2 in MAC
Expected pCO2 [kPa]= (HCO3act/5)+1 [range ±0.3kPa]

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 Problem 2 in classical approach

• Inadequate in complex disorders

• Only final result is seen, two or more disorders

may compensate/correct each other

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 Electroneutrality

• Answer to complex disorder

• Concept of electroneutrality emphasized
mostly by Peter Stewart
• Anion and cations in plasma must equal and
most of them can be measured
• This provides new insight into acid-base
situation in complex cases

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 Principle of electroneutrality
5 Other cations Alb-, P- 14 Albumin 3mM of neg.
SID 40 charge per 10g/l
HCO3- 25

strong anions 5

140 100
Na+
Cl-

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 Complex disease

• Try to imagine situation in patient’s plasma:

• Na-Cl (e.g. 140-106 = 34) (41) must be filled
with
– Weak acids (phosphate and albumin: 3mM/10g) =
(approx. 12 mM)
– Bicarbonate (25mM)
– The rest is eventually unmeasured strong acid
(normally <4 mM)

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 Look at ions and estimate SIDa
1
influence
SID ~ + -
[Na ]-[Cl ]
Normal value of [Na+]-[Cl-] = 34 mM
[Na+]-[Cl-] >> 34 = High SID alkalosis
[Na+]-[Cl-] << 34 = Low SID alkalosis

Quantitatively = deviation from 34 = BE attributable

to SID changes
Example: [Na+]-[Cl-] = 24 mM leads to BE -10mM if no other disorder

(D. Story, BJA 2004 / modified by J. Mallat 2017)

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 Limitations

• Other cations can distort SID estimation from

[Na+]-[Cl-]
– Measured: K+
– Measurable: Li+
– Unmeasurable: polymyxine antibiotics

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60
50
40 SID

Bland-Altman plot SIDa Na-Cl

14
30

Difference (SIDa-Na_Cl)

12
10
8
20

6
4
0 5 10 15 20 25 30 35 40 45 50 55 60
Average of SIDa and Na_Cl
10

0 10 20 30 40 50
Na-Cl [mmol/L] (Courtesy of Waldauf and Elbers)

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 Limitations

• Other cations can distort SID estimation from

[Na+]-[Cl-]
– Measured: K+
– Measurable: Li+
– Unmeasurable: polymyxine antibiotics
• A- estimation from Albumin can be inaccurate
– pH influences charge
– Neglects presence of phosphate, citrate and
paraproteins
• Lack of model validation

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 This explains

• Low albumin causes alkalosis

– BE +3 mM for each 10g/l of albumin missing
– Missing neg. charge on Albumin creates “more
space” for bicarbonate within SID
• Hyperchloridaemia causes acidosis
– 1mM extra chloride squeezes space for
bicarbonate (as space occupied by negative
charges of albumin is fixed)
– Indeed, what really matters is Na-Cl difference

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 This explains (cont.)

• Concentrational alkalosis/dilutional acidosis:

– If patient with diabetes insipidus loses H2O:
• Na increases from 140 to 160 (+14%) and Cl 100 to 114
(+14%), SIG increases from 40 to 46 mM (i.e. by 6mM)
• Albumin raises from 40 to 46 g/l (+14%), so it declares
cca 1.5 mM of this SID space (3mM per 10 g/L)
• It means that HCO3 (and BE) increases by 6-1.5=4.5
mM
– Dilution of ECF causes acidosis

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 Back to our case
28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
functions are stable. Abdomen soft and non-tender

• GI bleed?
• Alcoholic hepatitis and liver failure?
• Poisoning (e.g. ethylenglycol, methanol)?
• Other
– Gastroenteritis/food poisoning dehydration
– Non-diabetic ketoacidosis

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28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
functions are stable. Abdomen soft and non-tender

Sodium 132 mmol/L Arterial Blood Gas. 15 L/min O2 via

face mask
Potassium 4.6 mmol/L pH 7.432
Chloride 70 mmol/L pO2 28.3 kPa (212 mmHg)
Ionized Calcium 0.61 mmol/L pCO2 4.81 kPa (36 mmHg)
HCO3- (st) 24.3 mmol/L
BE -0.7 mmol/L
Glucose 8.0 144
mmol/L mg/dL
Haemoglobin 12 g/dL (120 g/L)
Describe acid-base disorder and give
possible causes.
Urine Ketones +
Glucose -

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 28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
functions are stable. Abdomen soft and non-tender

Sodium 132 mmol/L Arterial Blood Gas. 15 L/min O2 via face mask
Potassium 4.6 mmol/L pH 7.432
Chloride 70 mmol/L pO2 28.3 kPa (212 mmHg)
Ionized Calcium 0.61 mmol/L pCO2 4.81 kPa (36 mmHg)
HCO3- (st) 24.3 mmol/L
Base Excess -0.7 mmol/L
Glucose 8.0 mmol/L 144 mg/dL

Haemoglobin 12 g/dL (120 g/L) Describe acid-base disorder and give possible
causes.

Urine Ketones +
Glucose -

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 28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
functions are stable. Abdomen soft and non-tender

Sodium 132 mmol/L Arterial Blood Gas. 15 L/min O2 via

face mask
132-70 = 62 mM of space to be
pH 7.432
ocuppied by albumin and
Chloride 70 mmol/L pO2 28.3(normal
bicarbonate kPa (212 mmHg)
= 40)
pCO2 = HYPOCHLORIDEMIC
4.81 kPaALKALOSIS
(36 mmHg)
HCO3- (st)
expected BE +22 mM (or 24.3 mmol/L
more if
BE albumin is low)-0.7 mmol/L

Describe acid-base disorder and give

possible causes.

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 Situation in a patient
5 Other cations Alb-, P- 14 or less?

HCO3- 24.3

62
strong anions
There is also METABOLIC
132 ACIDOSIS caused by 22mM of
yet unknown strong anion.
Na+
70

Cl-

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 Concluding the case

• Low chloride is causing metabolic alkalosis

• This is matched by metabolic acidosis due to
unknown circulating anion
– Lactate (Type B of liver failure? Shock?)
– Renal failure (low Ca is suggestive high phosphate)
– (ketones)
– Poisons (e.g. ethylen glycol)

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 Answer sheet

• Combined hypochloridaemic alkalosis and

circulating anion (or high AG) acidosis

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 What it really was?

• Patient had acute-on-chronic liver failure due

to alcoholic hepatitis (MELD 37)
– Lactate 20.0 mmol/L, INR 3, bili 100 umol/l
– ALT 4908 IU/L (normal range <40)
• Akute kidney injury
– Crea 310 umol/l, urea 10.2mmol/l phosphate 3.08
mmol/l
• Died 20 hours after admission after being
refused by a transplant centre

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 Mental Algorithm Stage 2 (Intensivist)
Too high (>>34): MAL
hypochloridaemic or
• What disorder do you expect under the concentrational
Too low (<<34): MAC
circumstances? Is it there? hyperchloridaemic
• Assess compensation
• Examine these 3 components of bloods both
separately and whether they match
– Na-Cl difference (34) If there is still “space left”
it is filled by unexplained
– Charges on albumin (12) anions
– Bicarbonate (25)

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 In your mind

1 2 3 4 5
Look at BE
Look at Look at Look at
on blood Summarise
[Na+]-[Cl-] Albumin pCO2
gas

Compare with 10 g/L missing Identify strong If acidosis, it should Use clinical context
34 adds 3mM to ion, lactate be bicarb/5 + 1 kPa to unveil likely
BE and non- pathophysiology
lactate

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 Mental process

1 2 3 4 5
Disorders Identify
Disorders
caused by unmeasured Assess pCO2 Summarise
caused by A-
SID anion(s)

High SID Assess Compare BE Use „Bostron rule“,

metabolic influence on on BG strip eg. Winters
alkalosis, BE with BE formula
Predicted BE predicted,
+28 Look at lactate

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 Mental process

1 2 3 4 5
Disorders Identify
Disorders
caused by unmeasured Assess pCO2 Summarise
caused by A-
SID anion(s)

High SID Low albumin Compare BE Use „Bostron rule“,

metabolic alkalosis, on BG strip eg. Winters
alkalosis, Predicted BE +6 with BE formula
Predicted BE predicted,
+28 Look at lactate
BE = +34 mEq

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 Mental process

1 2 3 4 5
Disorders Identify
Disorders
caused by unmeasured Assess pCO2 Summarise
caused by A-
SID anion(s)

High SID Low albumin Lactic acidosis Use „Bostron rule“,

metabolic alkalosis, Predicted BE – 20 eg. Winters
alkalosis, Predicted BE +6 formula
Predicted BE Other strong ion
+28 acidosis
Predicted BE -14

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 Mental process

1 2 3 4 5
Disorders Identify
Disorders
caused by unmeasured Assess pCO2 Summarise
caused by A-
SID anion(s)

High SID Low albumin Lactic acidosis No respiratory

metabolic alkalosis, Predicted BE – 20 disorder
alkalosis, Predicted BE +6
Predicted BE Other strong ion
+28 acidosis
Predicted BE -14

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 Summarise and put into clinical
context

• High SID alkalosis

(BE +28)
• Low albumin (BE
+6)
• Strong anion
acidosis (BE -34)
– Lactate (BE-20)
– Unknown (BE -14)

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 Alternative approaches

• Low chloride or low albumin can mask circulating

anion
• There are other ways how to look at it:
– Albumin-corrected AG
– BE partitioning (D. Story, BJA 2004)
– Corrected chloride = 140/Na * Cl
• Compare with normal range 98-105 mM
– Strong ion gap (most precise, but need a calculator)

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 28 year old alcoholic presents with 3 days of nausea and
vomiting. He is confused, HR 134/min, but otherwise vital
Corrected Cl = 70*
functions are stable. Abdomen soft and non-tender
132/140= 74mM
i.e. 26mM lower than
should be, i.e. severe
Sodium 132 mmol/L Arterialhypochloridaemic
Blood Gas. 15 L/min
MAL, O2 via
face maskExpected BE +26
Potassium 4.6 mmol/L pH 7.432
Chloride 70 mmol/L pO2 28.3 kPa (212 mmHg)
Ionized Calcium 0.61 mmol/L pCO2 4.81 kPa (36 mmHg)
HCO3- (st) 24.3 mmol/L
BE -0.7 mmol/L
Glucose 8.0 144
mmol/L mg/dL
Haemoglobin 12 g/dL (120 g/L) AG=132+4-(24+70)=42 mM,
i.e.Describe
by 26mMacid-base
higher (ordistorder
more if and give
Alb is low)possible
than 16mM.
causes.
Urine Ketones + =Metabolic acidosis
Glucose -

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• Lets practice!

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 23 yr. old, 14 weeks pregnant presents with excessive
vomiting. First BG on presentation.

Sodium 133 mmol/L Arterial Blood Gas.

Potassium 3.4 mmol/L pH 7.316
Chloride 109 mmol/L pO2 17.0 kPa ( 128mmHg)
Ionized Calcium 1.3 mmol/L pCO2 1.99 kPa (15 mmHg)
HCO3- (st) 11.6 mmol/L
HCO3- (act) 7.6 mmol
BE -18.6 mmol/L
Albumin 22 g/L Lactate 0.7mM
Glucose 4.0 72mg/dL
mmol/L
Haemoglobin 9.3 g/dL (93 g/L)
Analyse components of acid-base
disorder and give possible causes.

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 Boston rule: 8/5+1=2.6 kPa
RESPIRATORY ALKALOSIS

Na-Cl=24 mM
HYPERCHLORIDAEMIC
ACIDOSIS

Alb=22g/L occupies 6mM,

bicarb 8, leaving 10mM for
unknown acid
HIGH AG ACIDOSIS

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 Expected answers

• Chronic compensated respiratory alkalosis of

pregnancy
• Acute high-AG acidosis
• Most likely ketoacidosis

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 Don’t give her normal saline

All other values in this patient kept constant (curve created on www.acidbase.org)

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• Another difficult one. Is it just a stroke?

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60 year old man with short bowel syndrome and
Boston rule CKD-IV
16/5+1= 4 kPa,sent
to A&E by GP for slurred speech and i.e.
ataxia. Diagnosis?
compensation OK, no
mixed disease

Na+ 152mM pH 7.350

K+ 5.0 mM pCO2 3.98 kPa (30 mmHg)
Cl- 115 mM HCO3 act 16.0 mM
Phosph/Ca2+ 1.9 mM/2.13mM BE - 8.5 mM
Urea 3.2 mM Glucose 4.2 mM (76 mg/dl)
Crea 312 µM Lactate 0.9 mM
Alb 30 g/L O/E: A: own
Osmolality 323 mosm/L B: RR 23, SpO2 99% on RA
LFT, ammonia Normal C: sinus 86/min, BP 140/86
WBR 4.8G/l D: E3M3V5, PEARL, no
meningeal or focal signs
CT brain Normal
E: NAD. BT 36.9. Urine dipstick
U toxicology Nil detected negative

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• Na-Cl=37 (OK, no hyperchloridaemia)
• Alb = 30 g/l, taking 9mM, phosphate
3mM, i.e. HCO3 should be 37-11=26mM
• HCO3 = 16 mM

This is HIGH AG ACIDOSIS – cca 10 mM of

acid in search

Lactate – normal
Ketones – negative
Renal failure ?
Poisons? Osm .gap normal (7 mM)

Neurology and short bowel is the key…

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 Expected answer

• D-lactic acidosis
• High AG acidosis/acidosis in AKD

• Real case: D-lactate confirmed 12.6mM,

patient improved on low-CHO diet

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 D-lactate

• Etiology: short bowel = unabsorbed glucose

enters colon = metabolized to D-lactate by colonic
bacteria (Lactobacillus sp.)= neurotoxicity
– Variable symptoms (“stroke-like”)
• Described by Oh et al. in 1979
• Htyte et al, 2011:
– 3% of in-hospital patients (2/3 after GI surgery), have
detectable D-lactate. Vast majority undiagnosed.
• Treatment = less CHO in diet, oral vancomycine

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 Lactate issue

• L-lactate is measured by POCT (BG machine)

• Usually correct, but:
– Probe can be faulty
– D-lactate not measured
– L-lactate can be falsely high (ethylene glycol
metabolites falsely detected as lactate)

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 Take home messages

• Electroneutrality is the key to understanding

complex AB disturbances
– Bicarbonate (BE) must fit with Na-Cl difference
and Albumin
– Albumin holds 3 mM of neg. charges per 10g/L,
and hypoalbuminaemia causes alkalosis
• In MAc, Boston rule allows to unveil
superposed respiratory disease
– Expected CO2 = Bicarb/5 + 1 [kPa]

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 In your mind

1 2 3 4 5
Look at BE
Look at Look at Look at
on blood Summarise
[Na+]-[Cl-] Albumin pCO2
gas

Compare with 10 g/L missing Identify strong If acidosis, it should Use clinical context
34 adds 3mM to ion, lactate be bicarb/5 + 1 kPa to unveil likely
BE and non- pathophysiology
lactate

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