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DOI-10.21304/2018.0504.00415

Postgraduate / Fellow Column

OSCE : Data Interpretation
Kundan Mittal*, Prashant Kumar**, Rajesh Mishra***, Vinayak Patki****
*Senior Professor, Department of Pediatrics, Incharge PICU and Respiratory Clinic,**Professor, Anaesthesia and Critical Care,
Pt B D Sharma, PGIMS Rohtak, Haryana, India ***Senior Intensivist, Ahmedabad, Gujarat, India, ****Chief Consultant, Advanced
Pediatric Critical Care Centre & Head, Dept of Pediatrics, Wanless Hospital, Miraj, Maharashtra, India
Received:22-Jul-18/ Accepted:05-Aug-18/Published Online:30-Aug-18

10 years old male child brought with history road-side • Haemoglobin 11.4gm/dL
accident when he was getting down from auto, a speedy • Ventilator Settings: PIP 19, PEEP 6, RR 18/min,
vehicle come from back side hit him from side. Child Ti o.9seconds, PS 10, Trigger 2L/min
became drowsy and had four episodes of vomiting and
Q. What is the diagnosis?
sustained following injuries; haemorrhagic contusion,
dislocation left clavicle, right kidney infarct, and Ans. A case of road side accident with severe traumatic
intraperitoneal haemorrhage, fracture both femur, brain injury, left clavicle dislocation, fracture both
hair-line cervical spine C5 fracture. His GCS was femur, right renal infarct with acute kidney injury
5/15, HR 56/min and BP 84/50mmHg, respiratory rate (decreased urine put and raised serum creatinine),
28/min irregular on arrival and later developed acute acute lung injury (PaO2/FiO2<300) acute liver injury
kidney injury. Child received Isolyte P, ceftriaxone (raised liver enzymes), acute muscle injury (raised
and linezolid beside supportive management. Urine CPK)hypotension (SBP <70 + Age x 2), impending
output decreased to 0.2mL/kg/hr for last 12 hours. His respiratory failure,altered sensorium (GCS <13/15),
lab reportsare as under. and possibility of raised ICP cannot be ruled out.
• Serum Sodium: 144mEq/L Q. What are the laboratory abnormalities?
• Serum Potassium: 5.2mEq/L Ans. Hypochloraemia, hypalbuminaemia, acute
kidney injury, hyperlactatemia, mild hyperkalaemia,
• Serum Chloride: 87mEq/L
acute lung injury, acute liver injury, acute muscle
• Serum Albumin: 44gm/L injury, suspected metabolic acidosis and alkalosis as
• Blood Urea: 62mg/dL per clinical details.
• Serum Creatinine: 2.1mg/dL Q. What are ABG abnormalities?
• Blood Glucose: 98mg/dL Normal Arterial-Blood Gas Values
• Serum Phosphate: 3.2mEq/L Parameter Arterial Mixed Peripheral
venous Venous
• Alkaline phosphatase: 172 IU/L
• Creatinine Kinase 4600 IU/L pH 7.36- 7.44 7.32- 7.36 7.32 – 7.38
• SGOT/SGPT: 862/1244IU/L
• pH 7.36 42-48
H+ 37-43 nEq/L
nEq/L
• PCO2: 40mmHg
23-30
• PaO2: 88mmHg HCO3- 22-26 mEq/L 24-30 mEq/L
mEq/L
• FiO2: 0.36 42-50
PCO2 35-45 mm Hg 44-46 mmHg
• Actual Bicarbonate: 22mEq/L mmHg
• Base Excess: -4
PaO2 80-100 mmHg 38-42 mmHg 40 mmHg
• Serum Lactate: 12mmol/L
Correspondence: >95% in room
Saturation >70% 65-75%
Dr. Kundan Mittal, Senior Professor Pediatrics, Pt B D Sharma, air
PGIMS, Rohtak Haryana, India,
Phone-+919416514111, Email-kundanmittal@gmail.com

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POST GRADUATE OSCE :Data Interpretation

1. Rule out lab error • Respiratory acidosis

PCO2 40 Acute (10min)=1 mEq ↑ in bicarbonate for
H = 24x ---------
+
45= 24x ------ =44 every 10 mmHg ↑ in PCO2 OR
HCO3- 22 ∆ HCO3- = 0.1 x PCO2
No lab error at pH 7.40 H concentration is 45
+ Chronic (3-5days) =3.5 mEq ↑ in bicarbonate
for every 10 mmHg ↑ in PCO2
RELATIONSHIP BETWEEN H+& pH
∆ HCO3- = 0.4 x ∆ PCO2
pH H+ pH H+
• Respiratory alkalosis
7.80 16 7.25 56
Acute (10min)=2 mEq ↓ in bicarbonate for
7.75 18 7.20 63
every 10 mmHg ↓ in PCO2
7.70 20 7.15 71
∆ HCO3- = 0.2 x ∆ PCO2
7.65 22 7.10 79
Chronic = 5 mEq ↓ in bicarbonate for every
7.60 25 7.00 89 10 mmHg ↓ in pCO2
7.55 28 6.95 100 ∆ HCO3- = 0.5 x PCO2
7.50 32 6.90 112 As such there is no compensation seen
7.45 35 6.85 141 5. Calculate base excess/deficit:
7.40 40 6.80 159 BE (mEq/L) = [(HCO3 −) − 24.4 + (2.3 ×
7.35 45 6.75 178 Hb + 7.7) × (pH − 7.4)] × 1– 0.023 × Hb]
(mEq/L), Hb in mmol/L
7.30 50 6.70 200
SBE = 0.9287 × [([(HCO3−) − 24 + 14.83 ×
2. Finding acidosis or alkalosis: (pH − 7.4)]
pH is in normal range so no acidosis or alkalosis. OR
Remember that normal pH does not mean that Acute change in 1.0mm/Hg PCO2 will change pH
there is no abnormality 0.008
3. Finding primary acid-base abnormality: Change of 0.01U pH result change in base of
HCO3 0.67mEq/L
pH = 6.1 + log ------------ Normal ration is 20/1 Next calculate measured pH & calculated pH
PCO2 x 0.03 Calculate the difference between calculated &
measured pH
Nearly normal
Multiply this pH with 67
4. Determine compensation:
No change seen
Metabolic acidosis= 1.2 mmHg ↓ in PCO2 for
6. What is anion gap (AG)?
every 1 mEq ↓ in bicarbonate. In acute stage up
to 8 hours and complete within 24hrs. Chronic • Anion gap exists because not all electrolytes
adaptation occurs in >24hours OR ∆ PCO2 = are routinely measured.
1.2 X ∆ HCO3-and expected PCO2 = 40-[1.2 x • Factors responsible for Anion Gap= UA
(24-current HCO3-)] [Albumin + alpha& beta globulin 15+ OA (5)
Last two digits corresponds to pCO2 value + PO4--- (2) + SO4-- (1)] =23
Metabolic alkalosis= 0.7 mmHg ↑ in PCO2 for UC [Ca++ (5) + K+ (4.5) + Mg++ (1.5)] = 11
every 1 mEq ↑ in bicarbonate. Chronic change • AG= Na++ K+ – (Cl-+ HCO3-)
>24hours OR ∆ PCO2 = 0.7 X ∆ HCO3-and Normal value: 12±4mEq/L (144+5.2) – (87
expected PCO2 = 40+[0.7 x (current HCO3- - + 22) = 40.2 (High anion gap Metabolic
24)] acidosis)

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POST GRADUATE
• Hydration induced conditions the ratio of
sodium and chloride will remain 1.4:1 or Cl-/
Na+ 0.75. Change in chloride without change
in sodium represents acid-base disorder.
Corrected chloride value can be calculated
as:measured chloride x 140/sodium.
• Actual bicarbonate level should be 42 but it
is not there. If bicarbonate rise to 42 mean
18 above normal then expected PCO2 will be
52 which is not there, indicates associated
respiratory alkalosis.
• One mmol of unmeasured acid titrates 1mmol
of bicarbonate
• Bicarbonate and chloride move in opposite
direction
• Bicarbonate was supposed to be 18 above
normal and chloride has decreased from
normal (97-107mEq/L)
• AG and HCO3- move opposite (AG/ HCO3–
1.5): (HCO3- 1 to 1.5)
• Calculating AG and HCO3- ratio one may
measure ECF for actual value
• Increase in anion gap above 20 is always
abnormal. In this case bicarbonate has not
decreased proportionately thus indicating
associated metabolic alkalosis.
• Increased lactate, hypalbuminaemia and
acute kidney injury are contributing towards
metabolic acidosis
• Final Diagnosis is metabolic acidosis with
metabolic alkalosis: Patient with acute kidney
injury can will have metabolic acidosis.
Persistent vomiting and inappropriate fluid
resuscitation may lead to metabolic alkalosis.
• Child has associated lactic acidosis
Q. What do we understand by corrected AG
(cAG)?
Ans. Albumin, phosphate and lactate levels are
used to calculate corrected AG since albumin and
phosphate constitute majority of anion.
(Na+ + K+) − (Cl− + HCO3− + 2[albumin g/
dL] + 0.5[phosphate mg/dL] + lactate)
Vol. 5 - No.4 Jul-Aug 2018
OSCE :Data Interpretation
OR
SI (all units mEq/L):(Na+ + K+) − (Cl− + HCO3− +
0.2[albumin g/L] + 1.5[phosphate mmol/L] + lactate)
Normal value: 0(±4 mEq/L)
Q. What are measured and calculated/derived
variables in ABG?
Ans. Measured variables are pH, PCO2, PaO2,
haemoglobin and derived variables are HCO3-, base
excess.
Q. What do we understand by Stewart’s concept
of acid-base?
Ans. Physiochemical or quantitative approach in which
plasma pH variation depends on water dissociation.
Thus, six major types of disorders can be defined on
the basis of Stewart’s approach. Acid is a substance
which increases water dissociation i.e. increases
H+production or bound with OH-. Change in pH can
be determined by three independent factors; SID,
arterial PCO2 and total weak acid concentration (Atot:
albumin and phosphate). When Atot increases then
H+ increases and vice versa. Bicarbonate isdependent
factor hence not involved in pH regulation. Urine SID
(sodium + potassium–chloride)is used to differentiate
acid-base abnormalities. When a fluid with different
SID of plasma (40 mEq/L) is given then its effect is
counter balanced by Atot and renal handling.
pH i.e. H+ depends on SID
SID (Normal 40 mEq/L) = Sodium + Potassium –
Chloride
SIDa= Sodium + Potassium + Calcium + Magnesium
- chloride + lactate
SIDe(effective) = SID – CO2 + A {(2x (albumin, gm/
dl) + 0.5 x (phosphate gm/dl)
SIG = SIDa – SIDe (physiologically slightly positive)
Reduction in SID indicates acidosis OR
SIDa = (Na+ + K+ + Ca++ + Mg++) − (Cl− + lactate−) =
40 ± 2 mEq/L
SIDe = [HCO3−] + [albumin (g/L) × (0.123 × pH −
0.631)] + phosphorus
(mEq/L) × (0.309 × pH − 0.469)] = 40 ± 2 mEq/L
SIG = SIDa − SIDe = 2 ± 2 mEq/L
SID is not much useful in routine practice
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POST GRADUATE
Q. What is albumin gap?
Normal AG also depends on phosphate and albumin
AG = 0.2 x Albumin(gm/L)+ 1.5 (phosphate)
Albumin gap = 40-Albumin level/4
AG + Albumin gap= Actual anion gap
({4.4 - [observed serum albumin (g/dL)] × 0.25} +
AG) - [serum lactate (mmol/L)]
([Na] + [K] - [Cl] - [HCO3]) -(2 x albumin g/dL + 0.5
x phosphate mg/dL) - [lactate mmol/L]]
Q. Name few causes of high anion gap.
Ans. GOLD MARK: Methanol, ethanol, lactate,
cyanide, aspirin, ethylene glycol, ketones, oxyproline
Q. Treatment advised on the basis of ABG report
Ans. Maintain tissue perfusion and manage acute
kidney injury
Q. Do you need to infuse sodium bicarbonate?
Ans. No. There are limited indications to use sodium
bicarbonate in intensive care settings.
Q. What are the reasons for his conditions?
Ans. Trauma, hypoperfusion, hypoxia, renal injury,
liver injury, muscle trauma, inappropriate fluid
therapy and possibly raised CPK level.
Q. Tell us something about hyperlactatemia.
Ans. Increased lactate level (normal lactate level
0.5-1.5 mmmol/L and half-life 10min; production
exceeds consumption may be as result of
hypoperfusion and microcirculatory dysfunction,
hypoxia (global or localised), renal injury, associated
gut injury, aerobic glycolysis, extensive trauma,
severe sepsis, propofol, antiretroviral agents, acute
How to cite this article:
Mittal K, Kumar P, Mishra R, Patki V. Postgraduate /Fellow Column-OSCE:Data Interpretation. J Pediatr Crit Care 2018;5(4):79-
82.
How to cite this URL:
Mittal K, Kumar P, Mishra R, Patki V. Postgraduate /Fellow Column-OSCE: Data Interpretation. J Pediatr Crit Care 2018;5(4):79-
82.. Available from: http://jpcc.in/userfiles/2018/0504-jpcc-jul-aug-2018/JPCC0504012.html
Vol. 5 - No.4 Jul-Aug 2018
OSCE :Data Interpretation
fulminant liver disease, severe anemia, diabetes
mellitus, salicylates toxicity, beta2 agonist. There are
two types of lactic acidosis; type A (associated with
tissue hypoxia), type B (Type B1 related to systemic
illness and type B2 related to poisoning and type B3
associated with increase in oxygen demand. Usually
raised anion gap and lactic acidosis go hand to hand
but may not always be true. Treatment includes
supporting circulation (maintaining perfusion,
adequate microcirculation), ventilation and targeting
etiology based therapy. Hyperlactatemia is good
marker of poor prognosis (>4mmol/L) and also
reflects metabolic adaptive response.
Q. What is the etiology of increased lactate level in
present case?
Ans. Possible causes are extensive traumatic injury,
hypoperfusion, renal injury, hypoperfusion, hypoxia,
liver injury, linezolid.
Q What are the risk factors of acute kidney injury
in present case?
Ans. In present case acute renal injury may be as a
result of direct trauma to kidney tissue, hypoperfusion
and high CPK level. Child is on ventilator and
high PEEP and sepsis may also contribute to renal
injury. CPK elevations are frequently classified as
mild, moderate, or severe [Mild less than 10 times the
upper limit of normal (or 2,000 IU/L), Moderate 10
to 50 times the upper limit of normal (or 2,000 IU/L
to 10,000 IU/L), and Severe greater than 50 times the
upper limit of normal]. High level may be associated
with acute kidney injury.
Conflict of Interest : Nil
Source of Funding : Nil
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