A 45-year-old man is admitted to the Emergency Department after ingesting an unknown quantity of “headache tablets”. His initial complaints are nausea, vomiting, shortness of breath and tinnitus. Fluid resuscitation has been commenced. You are asked to assess him as he is getting more dyspnoeic.
His serum biochemistry and arterial blood gas profile are as follows:
Parameter |
Result |
Normal Range |
Sodium |
138 mmol/L |
135 – 145 |
Potassium |
3.2 mmol/L* |
3.4 – 5.0 |
Chloride |
108 mmol/L |
100 – 110 |
Bicarbonate |
10 mmol/L* |
22 – 27 |
FiO2 |
0.3 |
|
pH |
7.32* |
7.35 – 7.45 |
PO2 |
125 mmHg (16.4 kPa) |
|
PCO2 |
20 mmHg (2.6 kPa)* |
35 – 45 (4.6 – 6.0) |
Base Excess |
-10 mmol/L* |
-2 – +2 |
Salicylate level |
105 mg/dL* |
3 – 10 mg/dL |
Paracetamol level |
<20 mg/L (<130 µmol/L) |
<20 (<130 µmol/L) |
a)
Acid-base status:
b)
c)
Hypoprothrombinaemia
Vitamin K
d)
Forced alkaline diuresis. Renal excretion of salicylates becomes important when the metabolic pathways become saturated. There is a 10-20 fold increase in elimination when the urine pH increased from 5 to 8
Haemodialysis. Most of the drug is protein-bound, and is concentration dependant. The volume of distribution is small, and binding site saturation leads to large levels of free drug, which is easily dialysable
Multiple-dose charcoal. Many aspirin forms are slow release and after ingestion they clump together in the GI tract, forming a large slow release preparation. It is also poorly soluble in the stomach leading to delayed absorption.
a)
The change in anion gap is 10, and the drop in bicarbonate is 14, which gives a delta ratio of 0.8, suggesting that there is a mixed high anion gap and normal anion gap metabolic acidosis.
There is indeed a respiratory alkalosis, which is appropriate (the rules of compensation suggest that the CO2 should be about 23).
b)
Salicylate toxicity has a whole list of complications. The college had asked specifically for severe ones. One may conceive of a respiratory alkalosis so dramatic as to warrant this adjective, and the same can be said for just about any other complication of salicylate toxicity, so they are all listed here.
Serum level 30-50mg/dL: | Serum level 50-75mg/dL: | Serum level >75mg/dL: |
|
|
|
c)
It is known that salicylate toxicity can cause a decrease in prothrombin.
Vitamin K (if not prothrombinex) is the answer.
d)
Severe toxicity from salicylates has several treatment options:
Decontamination
Direct and indirect antidotes
Enhancement of clearance
Supportive ICU therapies
O'Malley, Gerald F. "Emergency department management of the salicylate-poisoned patient." Emergency medicine clinics of North America 25.2 (2007): 333-346.
Pinedo, H. M., L. B. van de Putte, and E. A. Loeliger. "Salicylate-induced consumption coagulopathy." Annals of the rheumatic diseases 32.1 (1973): 66.
Shapiro, Shepard, Milton H. Redish, and Harold A. Campbell. "Studies on Prothrombin: IV. The Prothrombinopenic Effect of Salicylate in Man."Experimental Biology and Medicine 53.2 (1943): 251-254.
Pearlman, Brian L., and Rashi Gambhir. "Salicylate Intoxication." Postgraduate medicine 121.4 (2009).