After providing Miranda’s toxicology report and asking Claude.ai to analyze the data and present it as if in a court of law, the LLM bot generated this courtroom-appropriate explanation of the toxicological findings.

Speaking as Dr. Medical Examiner in testimony, Claude.ai states…

Your Honor, I have reviewed the complete toxicology report for Miranda Rose Souvannavong, and I will explain the significance of each drug found in her system, comparing the detected levels to what we would expect to see in therapeutic versus toxic ranges.

My key findings are as follows:

Bupropion (Wellbutrin) is an antidepressant. The therapeutic range for effectiveness is typically 50-100 ng/mL, with virtually no response below 25 ng/mL. Ms. Souvannavong’s level of 650 ng/mL is significantly elevated – approximately 6-13 times the therapeutic level. However, this falls well below the toxic range, as fatal overdoses typically show levels of 4,000-13,000 ng/mL.

Sertraline (Zoloft) is also an antidepressant. Therapeutic levels range from 9-82 ng/mL for a standard 200mg daily dose. Her level of 700 ng/mL is roughly 8-75 times higher than therapeutic levels. Postmortem levels above 1,500 ng/mL are considered potentially contributory to death, so her level approaches this concerning threshold.

Diazepam (Valium) is a benzodiazepine drug often used for the immediate control of anxiety symptoms. Therapeutic levels typically range from 100-400 ng/mL for chronic use. Her level of 120 ng/mL falls within the lower end of the normal therapeutic range, indicating appropriate prescribed use.

Mitragynine (Kratom) is the active component in kratom, an opioid-like substance often used to replace the use of the more unpredictable opioid drugs available for pain management. In three documented cases where mitragynine was ruled as the sole cause of death, levels ranged from 1,590-3,420 ng/mL. Ms. Souvannavong’s level of 820 ng/mL is approximately half the lowest fatal level reported.

Pseudoephedrine is a decongestant that showed a significantly elevated level. Normal therapeutic levels after a 60mg dose average around 200 ng/mL, and after 180mg around 800 ng/mL. Her level of 2,000 ng/mL is 2.5-10 times therapeutic levels. One fatal case reported a level of 19,000 ng/mL, so while elevated, this is not in the clearly lethal range.

Amphetamine is a stimulant and showed a level consistent with therapeutic use. Normal therapeutic peak levels range from 40-100 ng/mL, so 74 ng/mL falls within expected therapeutic range.

The decedent had multiple prescription medications in her system, with several at levels significantly above therapeutic ranges, particularly the antidepressants sertraline and bupropion, and the kratom alkaloid mitragynine. None of these levels alone reached fatal concentrations. The combination of these central nervous system depressants, along with her underlying pneumonia, may have contributed to respiratory depression and ultimately her demise from natural causes.

However, Your Honor, based on my analysis of both the autopsy findings and the toxicology results, I can offer several more probable medical explanations for these elevated drug levels. The most significant factor in elevated levels is postmortem redistribution. After death, drugs stored in tissues migrate back into the blood, artificially elevating concentrations. Several drugs found in Ms. Souvannavong’s system exhibit this phenomenon:

• Sertraline and Bupropion (the antidepressants) are highly lipophilic drugs that concentrate in tissues during life and redistribute postmortem
• Mitragynine can also redistribute after death
• Promethazine specifically exhibits postmortem redistribution, as noted in the toxicology report

A secondary factor is a compromised metabolism due to illness. Ms. Souvannavong’s severe bilateral lobar pneumonia would have significantly impacted her body’s ability to process medications. First, because of liver compromise. The autopsy revealed hepatic steatosis (fatty liver), weighing 2,780 grams, which is enlarged. The liver metabolizes most of the listed medications. Compromised liver function during her illness would slow drug clearance.

Second, kidney function deterioration. Her kidneys showed pale discoloration, suggesting probable compromise. Several of these drugs rely on kidney function for elimination.

An additional factor that would cause elevated levels postmortem is circulation restriction. Severe pneumonia causes poor oxygenation and circulation, further impairing the body’s ability to metabolize and eliminate drugs.

Tertiary factors for elevated levels are the decedent’s chronic pain and depression. The autopsy notes chronic regional pain syndrome and a spinal cord stimulator, showing she was managing significantly high levels of chronic pain. Patients with chronic conditions often take medications more frequently during illness exacerbations and have altered drug metabolism because of chronic disease, as well as increased tolerance to drugs, requiring higher doses.

Based on these extenuating factors, I must conclude that the elevated levels likely represent a combination of normal therapeutic dosing complicated by illness-impaired metabolism, with significant postmortem redistribution occurring after death. These levels do not show overdose or suicidal intent as much as they reveal the natural consequence of taking prescribed medications while severely ill with pneumonia.

This analysis supports the determination that her death was natural, caused by bilateral lobar pneumonia, with the drug levels being consequential rather than causal.