Homicidal Paraquat Poisoning Following Ligature Strangulation

Abstract

We report a case of homicidal paraquat poisoning preceded by attempted manual strangulation. The poison had been forcibly ingested when the victim was unconscious due to pressure on the neck. The victim survived for ten days and died due to development of fibrosing alveolitis. The autopsy showed classic features of proliferative stages of paraquat poisoning and healing signs of ligature strangulation.

Introduction

An investigation into cases of poisoning is a very common encounter in medicolegal practice in Sri Lanka. The majority of cases are due to the self-ingestion of agrochemicals such as paraquat or organophosphorus compounds. The forcible ingestion of poison with homicidal intention is an extremely rare occurrence. The prevalence of homicidal poisoning in Sri Lanka is 0.8%, including a few confirmed cases of forcible ingestion of poison (1). An Indian study showed that poisons used in homicide were mainly organophosphates, aluminum phosphide, paraquat, and arsenic, where the perpetrators were first-degree relatives (2).

Case History

A 20-year-old woman was admitted to the intensive care unit of a tertiary care hospital following ingestion of paraquat. She was pronounced dead ten days later. On admission, she was semiconscious, and there were greenish stains of paraquat around her mouth and on her clothing. By the third day of admission, she recovered from acute signs of intoxication and made a statement to the police, according to which she had met her ex-boyfriend at a lonely place close to her residence in an attempt to force her to restore their relationship. When she did not agree to do so, the assailant took out a thread made of two shoelaces and strangled her causing her to lose consciousness. While recovering, she felt an intense burning sensation in her mouth and noticed a greenish fluid and stains around her face. The assailant was also found lying unconscious on the ground. Both of them were taken to the hospital by citizens of the area who approached the scene in response to the victim’s screaming for assistance. The assailant was pronounced dead on admission due to paraquat poisoning.

Autopsy Findings

The body was that of an average built female, 156 cm in height. There was subconjunctival ecchymosis in both eyes (Image 1) and a healing ligature mark around the middle of the neck (Image 2). The mark consisted of three overcrossing lines, 3 mm in width, and completely encircled the neck. The hyoid bone and the laryngeal skeleton were intact. No significant lesions were present in the underlying soft tissues apart from the mild fibrocellular inflammatory reaction. The brain was edematous and cyanosed. The tongue was ulcerated and covered with whitish-yellow slough (Image 3). The esophageal mucosa was eroded and peeling off. The gastric mucosa appeared swollen. The liver showed extensive fatty changes with areas of focal necrosis. Both kidneys were pale and swollen, while the lungs were heavy, firm, emphysematous, and rubbery in consistency.

Image 1:

Subconjuctival Haemorrhages due to asphyxia

Image 2:

Ligature mark on the neck

Image 3:

Paraquat tongue

No postmortem toxicology was performed; in fact, according to our practical experience, toxicology has been found to be negative after one week of ingestion of paraquat. However, the paraquat was identified in the victim’s vomitus on admission using a spot test with analytical kits manufactured by Syngenta. Histopathology of the lung tissues showed signs of interstitial inflammation and hyaline membranes with fibrosing alveolitis (Images 4 and 5). The liver showed acute necrosis and fatty changes.

Image 4:

Interstitial inflammatory reaction with fibrosing alveolitis (H&E, x40).

Image 5:

Hyaline membranes, haemorrhages and interstitial inflammation of the lung (H&E, x100).

Cause of death was determined to be paraquat poisoning, proliferative stage, following attempted ligature strangulation.

Discussion

Paraquat is one of the most widely used herbicides in the world, which was first synthesized in 1882, but its herbicidal properties were not discovered until 1955. Paraquat is highly toxic to animals and has severe and irreversible delayed effects if absorbed. The minimum lethal dose by oral ingestion in human beings is approximately 35 mg/kg body weight, although a lesser quantity could be lethal without prompt treatment. Accidental or deliberate ingestion of paraquat has been responsible for a large number of pesticide-related deaths. It is a major suicide agent in many developing countries. In Sri Lanka, a 1989 study including 669 poison incidents indicated that agrochemicals were responsible for 59% of the incidents, and paraquat was the most common poisoning agent with a fatality rate of 68% (3). Ingestion of paraquat typically results in gastrointestinal illness, including oropharyngeal ulcerations, vomiting, and diarrhea, which might contain blood. Paraquat generates reactive oxygen species, which cause cellular damage via lipid peroxidation, activation of nuclear factor kappa-light-chain-enhancer of activated B cells, mitochondrial damage, and apoptosis in many organs. Patients might have dyspnea and hemoptysis as a result of pulmonary edema or hemorrhage, which can progress to fibrosis over the course of days to a couple of weeks (4). The presence of a burning sensation is said to be associated with high plasma-paraquat concentrations and is strongly predictive of fatal outcome (5).

In less severe cases, renal failure and gastrointestinal upset occur resulting in death within two or three days if untreated. Even if these complications are managed with hemodialysis and fluid resuscitation, pulmonary fibrosis progresses due to redox recycling (repetitive oxidation and reduction of the molecule, using up cellular energy) of paraquat in the lung. Death is then secondary to anoxia several days later; early oxygen treatment is thought to increase the risk of lung damage as it fuels the redox process (6). The use of activated charcoal, hemodialysis, immunosuppression with dexamethasone, cyclophosphamide, and antioxidant therapy are unlikely to change the clinical course (7). The history of circumstances and the autopsy findings of our case were characteristic of the proliferative stage of an acute paraquat poisoning.

The clinical examination of this patient during her stay in the hospital and also autopsy examination revealed a well-defined ligature mark around the neck with bilateral conjunctival hemorrhages. These findings are pathognomonic of asphyxia due to ligature strangulation. The application of pressure on the neck with tight ligature causes rapid unconsciousness and death is almost inevitable if pressure is maintained for a few minutes. The circumstances of this case suggest that the ligature had been used to incapacitate the victim and then the poison was poured into her mouth. In this context, toxic substances may aspirate and be absorbed through the respiratory passages as well. It is very unlikely, but not totally inconceivable, that the victim might have taken the poison on her own in an attempt to kill herself, applying a ligature around her neck in the form of complex suicide. Often homicidal forcible ingestion is preceded by either smothering or throttling (8). In a case of this nature, it is essential to prove that death was caused by poison administered with malicious or evil intent to the deceased. Premeditation was clearly evident here as the assailant was carrying a bottle of poison and a ligature to finish the victim if she did not comply. However, the case cannot be proven only by analytical findings or by autopsy findings but depends on the work of the criminal investigator at the scene of the crime and accounts of other witnesses (9). This proof must categorically eliminate the possibility that the death resulted from an accident, intentional substance abuse, or an act of suicide (10). The innate character of the crime of homicidal poisoning demands subterfuge and cunning. What is equally important is that there is usually a period of careful planning and also, not infrequently, the repetition of the act of administering poison (11). The detailed manner of administering poison cannot be revealed in this case due to the unconsciousness of the victim at the time of ingestion. A probe of the international forensic literature also failed to reveal any previously published epidemiological studies dealing with criminal investigative analysis, or psychological profiles of the homicidal poisoner (11).

Conclusions

This case showed a classic example of the two-stage homicide of a female victim, initially by ligature strangulation and then with forcible ingestion of poison. The proof of a case of similar nature demands thorough investigations into the circumstances in addition to autopsy and ancillary investigations.

Authors

Rohan Ruwanpura MD (Minsk) DLM MD(Col) DFM(RCPA) DMJ Clin et Path(Lond), Karapitiya Teaching Hospital - Forensic Medicine

Roles: Project conception and/or design, data acquisition, analysis and/or interpretation, manuscript creation and/or revision, approved final version for publication, accountable for all aspects of the work.

Chathura Nandasiri MBBS DLM MD(Col), Karapitiya Teaching Hospital - Forensic Medicine

Roles: Data acquisition, analysis and/or interpretation, manuscript creation and/or revision, approved final version for publication, accountable for all aspects of the work.