The absence of the parent chloral hydrate in the blood of Miss Smith suggests that her death did not occur immediately after a large ingestion/administration of the drug; due to the extremely short half-life of 4 minutes for chloral hydrate and since the chloral hydrate was a liquid preparation.
[snip]
Miss Smith had a peripheral blood TCE concentration of 75µg/mL and TCA concentration of 85µg/mL which is consistent with her having received repeated doses of chloral hydrate over a couple of days. A general therapeutic range for TCE is 2 to 12µg/mL
The TCE concentrations found in the blood, liver, brain, gastric and duodenal contents taken from Miss Smith are similar to literature concentrations (i.e., blood, 55µg/mL; brain, 91µg/g; liver, 200µg/g; and gastric, 5g) found in a fatality that occurred 3 hours after ingestion of chloral hydrate6.
[snip]
Serum and vitreous (eye fluid) chloride levels were elevated suggesting dehydration,
[snip]
This suggests that she took a significant dose of chloral hydrate in the hours preceding her death.
[snip]
j. Chloral hydrate may result in jaundice or icterus in cases of chronic toxicity. The absence of these findings suggests an overdose resulting in acute toxicity in this case.
b. If most cases of suicide, the victim ingests a large amount of a drug to insure death. The bottle found of chloral hydrate found near Miss Smith was only half empty.
c. In many case of prescription drug overdose, multiple drug levels are elevated. In this case, all drug, except chloral hydrate are at therapeutic levels.
http://www.broward.org/medical/investigative_report.pdf
1) the autopsy report did not prove chronic long-term use of ch. Is this finding contrary to KE’s claims that she had been using it since Sep ‘06?
2) If Anna had ‘tea’ by her bed, and pedialyte in a baby bottle (huh?), why did she show signs of dehydration?
3) could the increased chloride level be an effect of potassium chloride?
The administration of oral potassium salts to persons with normal excretory mechanisms for potassium rarely causes serious hyperkalemia. However, if excretory mechanisms are impaired, or if potassium is administered too rapidly intravenously, potentially fatal hyperkalemia can result (see CONTRAINDICATIONS and WARNINGS). It is important to recognize that hyperkalemia is usually asymptomatic and may be manifested only by an increased serum potassium concentration (6.5-8.0 mEq/L) and characteristic electrocardiographic changes (peaking of T-waves, loss of P-wave, depression of S-T segment and prolongation of the QT interval). Late manifestations include muscle paralysis and cardiovascular collapse from cardiac arrest (9-12 mEq/L).
Potassium supplements are contraindicated in patients with hyperkalemia since a further increase in serum potassium concentration in such patients can produce cardiac arrest. Hyperkalemia may complicate any of the following conditions: chronic renal failure, systemic acidosis such as diabetic acidosis, acute dehydration, extensive tissue breakdown as in severe burns, adrenal insufficiency or the administration of a potassium-sparing diuretic (e.g., spironolactone, triamterene or amiloride) (see OVERDOSAGE).
http://www.rxlist.com/cgi/generic/klor-con_od.htm