b) A 67-year-old lady is transferred from a regional hospital to a tertiary referral centre with a diagnosis of septic shock from a urinary source. She has not improved despite 48 hours of treatment with antibiotics and supportive care.
Parameter |
Measured value |
Normal range |
Admission |
||
pH |
6.93* |
7.35-7.45 |
PaCO2 |
48* (6.3*) |
35-45 mmHg (4.6-6.0 kPa) |
PaO2 |
160 (21.0*) |
80-100 mmHg (10.5-13.0 kPa) |
Oxygen Saturation |
99.2 |
>95% |
HCO3 |
10* |
22-27 mmol/l |
Base Excess |
-22* |
-2 to +2 mmol/L |
Sodium |
123* |
135-145 mmol/l |
Potassium |
5.4* |
3.2-4.5 mmol/l |
Chloride |
95* |
100-110 mmol/l |
Glucose |
7.0* |
3.0-6.0 mmol/l |
Lactate |
2.8* |
< 2.0 mmol/l |
Urea |
33.0* |
3.5-7.2 mmol/l |
Creatinine |
541* |
50-100 ol/l |
i. Describe her biochemical profile on admission
ii. List the causes of a raised lactate in sepsis
i.
ii.
This question is a fairly straightforward ABG interpretation exercise.
There are many different reasons for why lactate might rise in sepsis. Apart from the shocked state, there is the catecholamine release, microvascular shunting, mitochondrial dysfunction due to pyruvate dehydrogenase inhibition, and diminished hepatic blood flow. I tried to explain this to myself in another chapter.
www.anaesthesiamcq, as always.
Jones, Alan E., and Michael A. Puskarich. "Sepsis-induced tissue hypoperfusion." Critical care clinics 25.4 (2009): 769.
Crouser, Elliott D. "Mitochondrial dysfunction in septic shock and multiple organ dysfunction syndrome." Mitochondrion 4.5 (2004): 729-741.
Levy, Bruno. "Lactate and shock state: the metabolic view." Current opinion in critical care 12.4 (2006): 315-321.
Bateman, Ryon M., Michael D. Sharpe, and Christopher G. Ellis. "Bench-to-bedside review: microvascular dysfunction in sepsis-hemodynamics, oxygen transport, and nitric oxide." CRITICAL CARE-LONDON- 7.5 (2003): 359-373.