Absence of GI symptoms within 6hr of ingestion excludes significant<unk>  ingestion (exception: enteric coated tablets)
Significant<unk>  can result in a severe lactic acidosis from hypoperfusion due to volume loss, vasodilation and negative inotropin effects.
Stage I: GI toxicity: nausea, vomiting, diarrhea, GI bleeding from local corrosive effects of<unk>  on the gastric and intestinal mucosa
Stage II: Quiescent phase with resolution of GI symptoms and apparent clinical improvement
controversy between toxicologists whether this stage exists in significant poisonings
Stage III: Systemic toxicity: shock and hypoperfusion
Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
GI fluid losses, increase capillary permeability, decreased venous tone
Severe anion gap acidosis
Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
Hepatotoxicity from<unk>  delivery via portal blood flow
Stage IV: Clinical recovery, resolution of shock and acidosis usually by days 3-4
Stage V: Late onset of gastric and pyloric strictures (2-8 week later) 
controversy between toxicologists whether this stage exists in significant poisonings
Primarily hypovolemic shock and acidosis, myocardial dysfunction also contributes
GI fluid losses, increase capillary permeability, decreased venous tone
Severe anion gap acidosis
Free radical damage to mitochondria disrupt oxidative phosphorylation which leads to lactic acidosis
Hepatotoxicity from<unk>  delivery via portal blood flow
Iron toxicity
Aluminum toxicity
Zinc toxicity
Antimony toxicity
Gold toxicity
Arsenic toxicity
Nickel toxicity
Barium toxicity