A 45-year-old male 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 |
Patient Value |
Normal Adult 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 |
|
Paracetamol level |
< 20 mg/L (< 130 µmol/L) |
< 20 (< 130) |
a) Describe the acid-base status. (20% marks)
b) What are four severe complications of this toxidrome? (20% marks)
c) What coagulopathy may be present in this toxidrome and what is the treatment? (10% marks)
d) What are the treatment options for severe toxicity, and what is their rationale? (50% marks)
a)
Acid-base status:
Increased anion gap metabolic acidosis Concomitant normal anion gap metabolic acidosis Respiratory alkalosis
Decreased delta ratio
b) Hypoglycaemia
Pulmonary oedema Cerebral oedema Arrhythmias Hyperpyrexia
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 dialyzable.
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.
Additional Examiners’ Comments:
Most candidates understood the acid-base abnormalities but not all were able to provide cogent answers relating to the complications and management. Few were able to describe all the treatment options for severe toxicity with the rationale for these strategies.
This question is identical to Question 10 from the second paper of 2012.
b) Complicatons of salicylate overdose:
Serum level 30-50mg/dL: | Serum level 50-75mg/dL: | Serum level >75mg/dL: |
|
|
|
b) Coagulopathy in salicylate overdose? Its not just platelet inhibition. According to UpToDate, this is because of hepatotoxicity and interference with the synthesis of vitamin K dependent factors. Specifically, it is well known that salicylate toxicity can cause a decrease in prothrombin. Vitamin K (if not prothrombinex) is the answer.
c)Management of sever salicylate overdose consists of the following measures:
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).