ASA level
Acetaminophen level (possible co-ingestant)
Metabolic panel
Renal failure prevents ASA clearance
Hyperglycemia in periphery (CSF will have low glucose due to CNS hypermetabolic state)
Hypokalemia requires aggressive repletion - this differentiates from DKA which tends to have hyperkalemia or normokalemia at initial presentation
Urinary alkalinization inhibited by excretion of H+ in order to reabsorb K+
Mag and phos
Urine toxicology screen
Urinalysis
VBG
CBC
PTT, PT/INR
LFTs
ECG
Chest and abdominal radiographs
Renal failure prevents ASA clearance
Hyperglycemia in periphery (CSF will have low glucose due to CNS hypermetabolic state)
Hypokalemia requires aggressive repletion - this differentiates from DKA which tends to have hyperkalemia or normokalemia at initial presentation
Urinary alkalinization inhibited by excretion of H+ in order to reabsorb K+
Urinary alkalinization inhibited by excretion of H+ in order to reabsorb K+
Triple-mixed acid-base disturbance
Respiratory alkalosis (earliest sign), AG metabolic acidosis, metabolic (contraction) alkalosis
Only other entity that produces this pattern is sepsis
Elevated ASA level
Obtain levels q1-2hr until levels decline and patient's clinical status stabilizes
May be deceptively low early after ingestion and with chronic<unk> 
Respiratory alkalosis (earliest sign), AG metabolic acidosis, metabolic (contraction) alkalosis
Only other entity that produces this pattern is sepsis
Obtain levels q1-2hr until levels decline and patient's clinical status stabilizes
May be deceptively low early after ingestion and with chronic<unk> 
Therapeutic: 10-30mg/dL<unk> : >40-50mg/dL
Rapidly absorbed - measurable levels in 30 minutes
Peak occurs ~6hr after absorption (up to 60hr if enteric-coated or extended release)
Salicylate toxicity
Lactic acidosis
Chlorate toxicity
Sepsis, shock, liver disease, CO, CN, metformin, methemoglobin
Organophosphate toxicity
Short bowel syndrome
Thallium toxicity
Propylene glycol infusions for lorazepam and phenobarbital