Desseminated Intravascular Coagulopathy Caused By Acetic Acid Intoxication : A Case Report / 대한법의학회지

ABSTRACT

Strong corrosive acid is accidentally ingested by children or by psychiatric patients for the purpose of suicidal attempt. Late complications include chemical burn to pharyunx, perforation and stricture of upper gastrointestinal tract, respiratory insufficiencyand renal failure caused by hemoglobinuria following hemolysis. Acetic acid is difficult to ingestion large volume in a time because it is a strong irritant, provocating painful pharynx, and its autopsy case is rare. We report an autopsy case of acetic acid intoxication with acute disseminated intravascular coagulation (DIC) in several hours. We present pathogenesis of acetic acid intoxication and the associated forensic problems. A comatous 39-year-old female was admitted to emergency room 6 hours after she swallowed 90 gm of acetic acid. She was treated with gastric lavage but she was expired 9 hours after swallowing acetic acid. She was consulted to Department of Forensic Medicine of Kyungpook National University School of Medicine. She was grossly icteric and livor mortis was generally dark red. External wounds were 10 hemorrhagic lesions with 5 x 3.7cm and 3 x 2.8cm on the left arm and hand dorsum and facial abrasions. Internal gross examination revealed several purpural lesions in the gastric serosal surface and greater omentum. Microscopically, the stomach showed diffuse mucosal coagulation necrosis and intravascular hyalinized or fibrinoid thrombi in submucosal blood vessels. Liver showed necrosis of periportal area (zone I) and intracellular cholestasis around the central vein. Sections from renal tissue frequently show hemoglobin casts in the tubules and RBCs in the Bowman's capsules. Acetic acid of a remnant bottle, sampled blood and bloody necrotic tissues in the stomach were toxicologically examined in National Science Laboratory. The purity of ingested acetic acid is 98%, the concentration of acetic acid ion in blood is 734ppm and the content in gastric juice is 0.09%. In patients after acetic acid ingestion, DIC is most probably caused by procoagulants, produced by extensive acid-induced necrosis of the upper gastrointestinal tract. In this case, several purpural lesions were revealed on the arm, around facial abrasion and intravenous injection sites of the wrists. These are important to differentiate with contusion because she was battered before acetic acid ingestion. Purpurae in DIC are poorly demarcated, dark purple elevations with spreading margin but subcutaneous hemorrhage in contusion is grayish black or dark red with well demarcation (Table 2). But careful examination should be considered because traumatic hemorrhage is also exaggerated and mixed in DIC. (The Korean Journal of Legal Medicine)