J Forensic Sci, November 2014, Vol. 59, No. 6 doi: 10.1111/1556-4029.12538 Available online at: onlinelibrary.wiley.com
CASE REPORT PATHOLOGY / BIOLOGY
Isabella Aquila,1,†M.D.; Francesca Pepe,1,† M.D.; Ciro Di Nunzio,1 Ph.D., M.S.H.; Francesco Ausania,1 M.D.; Arianna Serra,1M.D.; and Pietrantonio Ricci,1M.D., Ph.D.
Suicide Case Due to Phosphoric Acid Ingestion: Case Report and Review of Literature*
ABSTRACT: Ingesting caustic substances represents a common event which may result in serious injuries of the gastrointestinal system.
Severity of injury depends on the type of ingested substance: Caustic burns are more frequently associated with acid ingestion and their severity depends on type, concentration, time of exposure, and amount of the ingested substance. We report a case of phosphoric acid ingestion leading to death in a patient with depressive disorder. While reports ingestion of other acids and organophosphates can be found in the literature, there are no reports detailing a death due to phosphoric acid ingestion. We hope that presenting the findings in this case can aid death investigators in future cases that may involve ingestion of such a substance. After autopsy pH, phosphate and calcium ions concentration in the blood were analyzed. The cause of death was due to systemic effects: metabolic acidosis, hypophosphatemia, hypocalcemia, and hyperkalemia.
KEYWORDS: forensic science, death, caustic substances, depressive disorder, ingestion, phosphoric acid Ingesting caustic substances represents a common event which may result in serious injuries of the gastrointestinal system (1–4). Severity of injury from caustic ingestion depends on the type of ingested substance. Acid ingestion may lead to early lethal complications (gastric perforation, massive metabolic acidosis) and long-term injuries such as pyloric stenosis. In addition to local complications (5), there are systemic problems such as respiratory failure, provoked by the direct contact of the substance on the mucosa respiratory tract, by inhalation and by edema of the glottis. Also, organs such as the liver and the pancreas are involved, eventually arriving at systemic multi-organ failure (6,7). Moreover, renal failure leads to reabsorption of toxins and hypovolemia, and eventually respiratory impairment ensues leading to adult respiratory distress syndrome, disseminated intravascular coagulation, and death (8). During acidosis, there is migration of phosphorus from inside the cells to the extracellular fluid, increasing serum phosphate levels, leading to heightened urinary losses of phosphate. During marked hyperphosphatemia, a portion of phosphate becomes non-ultrafilterable and forms colloidal complexes with calcium, leading to hypocalcemia (9). Case An 81-year-old woman committed suicide by ingesting detergent sanitizer containing phosphoric acid. Initially, the patient Chair of Legal Medicine, University “Magna Graecia” of Catanzaro, Viale Europa loc. Germaneto, 88100 Catanzaro, Italy. *Presented in part at the 22nd Congress of the International Academy of Legal Medicine, July 5-8, 2012, in Istanbul, Turkey. † These authors contributed equally to this manuscript. Received 15 Nov. 2012; and in revised form 17 July 2013; accepted 12 Oct. 2013. 1
© 2014 American Academy of Forensic Sciences
was in good condition with vital signs intact. The chest examination was negative, but noisy breathing was evident. There were also oral lesions and abdominal pain. The patient presented with impaired renal and cardiac function indexes, and there were also alterations of the electrolytes. The radiological examination of the abdomen identified air-fluid levels and gaseous distension of bowel loops and stomach. The patient then developed a state of shock and progressed into a state of stupor with worsening vital signs, respiratory failure requiring intubation, and eventually death. An autopsy was ordered. Materials and Methods After a careful review of the clinical history, we performed a complete autopsy including external, internal, and toxicological examinations. Toxicology testing included an automated immunoassay on an ILAB 600 Chemistry (Instrumentation Laboratory, Bedford, MA) to detect Ph, phosphate, and calcium ions concentration in the blood. Gastric and intestinal fluid were evaluated through HP 5890 Series II Plus GC system combined with a HP 5972 Series mass selective detector (Agilent Technologies, Deutschland, Germany), to detect any chemical substance in particular phosphoric acid. 10 mL of a blue liquid (thought to be the caustic substance ingested by woman) was investigated by the same method. The results of these analyses were compared. Results Autopsy examination showed an area of necrosis situated at the root of the tongue. The esophagus (Fig. 1) had edematous mucosa and an area of necrosis in the cervical tract. The trachea (Fig. 2) demonstrated a hyperemic mucosa with red mucus and multiple areas of necrosis. Both lungs displayed emphysema and 1665
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JOURNAL OF FORENSIC SCIENCES
FIG. 1––Edematous mucosa of esophagus.
FIG. 4––Thinning of the gastric mucosa.
FIG. 2––Hyperemic mucosa of trachea.
FIG. 5––Mucosal necrosis of intestine.
FIG. 3––Distension of the stomach.
FIG. 6––Opening of the intestine.
congestion. Upon squeezing the lungs, a mix of blood with a liquid foam was detected. The stomach (Fig. 3) was found intact but distended with an area of putrefaction and collection of black liquid in the greater curvature and thinning of the gastric mucosa (Fig. 4). The intestine had mucosal necrosis (Fig. 5), especially in the proximal tract. Opening of the intestine (Figs 6–7) exhibited a black material in the proximal tract and a green material emanating a soapy smell in the distal tract. There were signs of cerebral edema and congestion. Toxicological analysis of the blood showed a high concentration of phosphates (7.5 mg/dL) and a low concentration of calcium (2.6 mg/dL). Examination of gastric fluid again showed a high concentration of phosphates (31 mg/dL) as well as alkyl benzyl ammonium chloride and ethylated alcohol. Histological examination revealed congestion, edema, and acute inflammatory infiltrate at the base of the
FIG. 7––Green material in the distal tract of intestine.
AQUILA ET AL.
tongue and large areas of hemorrhagic and ulcerative necrosis in the digestive tract, especially in proximal portions. Discussion Phosphorus plays a major role in the cellular function. Phosphorus is present in the inorganic form in the extracellular fluid, and the kidneys play a major role in its regulation. During acidosis, there is movement of phosphorus from inside the cells to the extracellular zone, increasing serum phosphate levels (10,11). During hyperphosphatemia, phosphate ions develop colloidal complexes with calcium ions with the resulting serum hypocalcemia. The caustic action of phosphoric acid causes coagulation necrosis and ulceration of tissue. A review of the literature does not reveal any reports of death due to ingestion of phosphoric acid, although there are several cases of death due to organophosphate pesticides (12–14). Management of patients in these cases is complicated. There is a surgical treatment relating to damage from caustic ingestion and a pharmacological treatment for hyperphosphatemia and hypocalcemia (15–17). The long-term outcomes of these patients are not favorable. The results depend on the time between ingestion and the treatment and especially on the amount of the substance ingested. Conclusions In this case, the cause of death was cardio-respiratory failure resulting from acute metabolic acidosis with hypophosphatemia, hypocalcemia, and hyperkalemia due to ingestion of phosphoric acid. Examination revealed ulcerative and hemorrhagic coagulation necrosis of the upper portions of the digestive tract. Caustic lesions were found in the gastric and intestinal mucosa; however, the esophagus was protected presumably due to its alkalinity and the speed the liquid passed through. Furthermore, regarding the respiratory system, the phosphoric acid provoked glottis edema; mucosal necrosis of the pharynx, hypopharynx, and trachea; and increased pulmonary edema. The patient developed depression of the central nervous system and a fatal cardiac dysrhythmia due to the electrolyte abnormalities. The dysrhythmia was in part due to hyperkalemia, which can also cause depolarization of cell membranes and inexcitability of cells to a development of lethal dysrhythmias including ventricular fibrillation. In conclusion, not only did the ingestion of acid produced local gastro-intestinal and respiratory mucosa, but it also caused systemic effects such as metabolic acidosis, hypophosphatemia, hypocalcemia and hyperkalemia and eventually death.
.
SUICIDE CASE DUE TO PHOSPHORIC ACID INGESTION
1667
References 1. Lupa M, Magne L, Lindhe Guarisco J, Amedee R. Update on the diagnosis and treatment of caustic ingestion. Ochsner J 2009;9:54–9. 2. Bureau of Policy and Strategy, Ministry of Public Health. Health statistic. Thailand Health Profile 2001-2004; http://www.moph.go.th/ops/ health_48 (accessed July 12, 2013). 3. Watson WA, Litovitz TL, Rodgers GC Jr, Klein-Schwartz W, Reid N, Youniss J, et al. 2004 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2005;23:589–666. 4. Vijayanath V, Nagaraja RK, Raju GM, Anitha MR. Forensic issues in suicide due to acid ingestion in a case of major depressive disorder. Am J Forensic Med Pathol 2012;33(2):156–8. 5. Pace F, Antinori F, Repici A. What is new in esophageal injury (infection, drug-induced, caustic, stricture, perforation)? Curr Opin Gastroenterol 2009;25:372–9. 6. Ashcraft KW, Padula RT. The effect of dilute corrosive of the esophagus. Pediatrics 1974;53:226–32. 7. Haller JA Jr, Andrews HG, White JJ, Tamer MA, Cleveland WW. Pathophysiology and management of acute corrosive burns of the esophagus: results of treatment in 285 children. J Pediatr Surg 1971;6:578–84. 8. Caravati EM. Metabolic abnormalities associated with phosphoric acid ingestion. Ann Emerg Med 1987;16:904–6. 9. Hebert LA, Lemann J Jr, Petersen JR, Lennon EJ. Studies of the mechanism by which phosphate infusion lowers serum calcium concentration. J Clin Invest 1966;45:1886–94. 10. Friedman EM. Caustic Ingestion and foreign bodies in the aerodigestive tract of children. Pediatr Clin North Am 1989;36(6):1403–10. 11. Slatopolsky E, Rutherford WE, Rosenbaum R, Martin K, Hruska K. Hyperphosphatemia. Clin Nephrol 1977;7:138–46. 12. Tanaka T, Tanaka N, Kita T, Kasai K, Sato HJ. Acephate in biological fluids of two autopsy cases after ingestion of the chemical. J Forensic Sci 2005;50(4):933–6. 13. Kamenczak A, Jasinska-Kolawa K, Targosz D, Szkolnicka B, Sancewicz-Pach K. Acute pesticides poisoning in the Krakow Department of Clinical Toxicology in 1986-1995. Przegl Lek 1997;54(10):671–6. 14. Aardema H, Meertens JH, Ligtenberg JJ, Peters-Polman OM, Tulleken JE, Zijlstra JG. Organophosphorus pesticide poisoning: cases and developments. Neth J Med 2008;66(4):149–53. 15. Harlak A, Yigit T, Coskun K, Ozer T, Mentes O, G€ulec B, et al. Surgical treatment of caustic esophageal strictures in adults. Int J Surg 2013;11(2):164–8. 16. Chirica M, Resche-Rigon M, Bongrand NM, Zohar S, Halimi B, Gornet JM, et al. Surgery for caustic injuries of the upper gastrointestinal tract. Ann Surg 2012;256(6):994–1001. 17. Cakal B, Akbal E, K€okl€u S, Babalı A, Kocßak E, Tasß A. Acute therapy with intravenous omeprazole on caustic esophageal injury: a prospective case series. Dis Esophagus 2013;26(1):22–6. Additional information and reprint requests: Isabella Aquila, M.D. Chair of Legal Medicine University Magna Graecia of Catanzaro Viale Europa loc. Germaneto 88100 Catanzaro Italy E-mail: [email protected]
CASE REPORT PATHOLOGY / BIOLOGY
Isabella Aquila,1,†M.D.; Francesca Pepe,1,† M.D.; Ciro Di Nunzio,1 Ph.D., M.S.H.; Francesco Ausania,1 M.D.; Arianna Serra,1M.D.; and Pietrantonio Ricci,1M.D., Ph.D.
Suicide Case Due to Phosphoric Acid Ingestion: Case Report and Review of Literature*
ABSTRACT: Ingesting caustic substances represents a common event which may result in serious injuries of the gastrointestinal system.
Severity of injury depends on the type of ingested substance: Caustic burns are more frequently associated with acid ingestion and their severity depends on type, concentration, time of exposure, and amount of the ingested substance. We report a case of phosphoric acid ingestion leading to death in a patient with depressive disorder. While reports ingestion of other acids and organophosphates can be found in the literature, there are no reports detailing a death due to phosphoric acid ingestion. We hope that presenting the findings in this case can aid death investigators in future cases that may involve ingestion of such a substance. After autopsy pH, phosphate and calcium ions concentration in the blood were analyzed. The cause of death was due to systemic effects: metabolic acidosis, hypophosphatemia, hypocalcemia, and hyperkalemia.
KEYWORDS: forensic science, death, caustic substances, depressive disorder, ingestion, phosphoric acid Ingesting caustic substances represents a common event which may result in serious injuries of the gastrointestinal system (1–4). Severity of injury from caustic ingestion depends on the type of ingested substance. Acid ingestion may lead to early lethal complications (gastric perforation, massive metabolic acidosis) and long-term injuries such as pyloric stenosis. In addition to local complications (5), there are systemic problems such as respiratory failure, provoked by the direct contact of the substance on the mucosa respiratory tract, by inhalation and by edema of the glottis. Also, organs such as the liver and the pancreas are involved, eventually arriving at systemic multi-organ failure (6,7). Moreover, renal failure leads to reabsorption of toxins and hypovolemia, and eventually respiratory impairment ensues leading to adult respiratory distress syndrome, disseminated intravascular coagulation, and death (8). During acidosis, there is migration of phosphorus from inside the cells to the extracellular fluid, increasing serum phosphate levels, leading to heightened urinary losses of phosphate. During marked hyperphosphatemia, a portion of phosphate becomes non-ultrafilterable and forms colloidal complexes with calcium, leading to hypocalcemia (9). Case An 81-year-old woman committed suicide by ingesting detergent sanitizer containing phosphoric acid. Initially, the patient Chair of Legal Medicine, University “Magna Graecia” of Catanzaro, Viale Europa loc. Germaneto, 88100 Catanzaro, Italy. *Presented in part at the 22nd Congress of the International Academy of Legal Medicine, July 5-8, 2012, in Istanbul, Turkey. † These authors contributed equally to this manuscript. Received 15 Nov. 2012; and in revised form 17 July 2013; accepted 12 Oct. 2013. 1
© 2014 American Academy of Forensic Sciences
was in good condition with vital signs intact. The chest examination was negative, but noisy breathing was evident. There were also oral lesions and abdominal pain. The patient presented with impaired renal and cardiac function indexes, and there were also alterations of the electrolytes. The radiological examination of the abdomen identified air-fluid levels and gaseous distension of bowel loops and stomach. The patient then developed a state of shock and progressed into a state of stupor with worsening vital signs, respiratory failure requiring intubation, and eventually death. An autopsy was ordered. Materials and Methods After a careful review of the clinical history, we performed a complete autopsy including external, internal, and toxicological examinations. Toxicology testing included an automated immunoassay on an ILAB 600 Chemistry (Instrumentation Laboratory, Bedford, MA) to detect Ph, phosphate, and calcium ions concentration in the blood. Gastric and intestinal fluid were evaluated through HP 5890 Series II Plus GC system combined with a HP 5972 Series mass selective detector (Agilent Technologies, Deutschland, Germany), to detect any chemical substance in particular phosphoric acid. 10 mL of a blue liquid (thought to be the caustic substance ingested by woman) was investigated by the same method. The results of these analyses were compared. Results Autopsy examination showed an area of necrosis situated at the root of the tongue. The esophagus (Fig. 1) had edematous mucosa and an area of necrosis in the cervical tract. The trachea (Fig. 2) demonstrated a hyperemic mucosa with red mucus and multiple areas of necrosis. Both lungs displayed emphysema and 1665
1666
JOURNAL OF FORENSIC SCIENCES
FIG. 1––Edematous mucosa of esophagus.
FIG. 4––Thinning of the gastric mucosa.
FIG. 2––Hyperemic mucosa of trachea.
FIG. 5––Mucosal necrosis of intestine.
FIG. 3––Distension of the stomach.
FIG. 6––Opening of the intestine.
congestion. Upon squeezing the lungs, a mix of blood with a liquid foam was detected. The stomach (Fig. 3) was found intact but distended with an area of putrefaction and collection of black liquid in the greater curvature and thinning of the gastric mucosa (Fig. 4). The intestine had mucosal necrosis (Fig. 5), especially in the proximal tract. Opening of the intestine (Figs 6–7) exhibited a black material in the proximal tract and a green material emanating a soapy smell in the distal tract. There were signs of cerebral edema and congestion. Toxicological analysis of the blood showed a high concentration of phosphates (7.5 mg/dL) and a low concentration of calcium (2.6 mg/dL). Examination of gastric fluid again showed a high concentration of phosphates (31 mg/dL) as well as alkyl benzyl ammonium chloride and ethylated alcohol. Histological examination revealed congestion, edema, and acute inflammatory infiltrate at the base of the
FIG. 7––Green material in the distal tract of intestine.
AQUILA ET AL.
tongue and large areas of hemorrhagic and ulcerative necrosis in the digestive tract, especially in proximal portions. Discussion Phosphorus plays a major role in the cellular function. Phosphorus is present in the inorganic form in the extracellular fluid, and the kidneys play a major role in its regulation. During acidosis, there is movement of phosphorus from inside the cells to the extracellular zone, increasing serum phosphate levels (10,11). During hyperphosphatemia, phosphate ions develop colloidal complexes with calcium ions with the resulting serum hypocalcemia. The caustic action of phosphoric acid causes coagulation necrosis and ulceration of tissue. A review of the literature does not reveal any reports of death due to ingestion of phosphoric acid, although there are several cases of death due to organophosphate pesticides (12–14). Management of patients in these cases is complicated. There is a surgical treatment relating to damage from caustic ingestion and a pharmacological treatment for hyperphosphatemia and hypocalcemia (15–17). The long-term outcomes of these patients are not favorable. The results depend on the time between ingestion and the treatment and especially on the amount of the substance ingested. Conclusions In this case, the cause of death was cardio-respiratory failure resulting from acute metabolic acidosis with hypophosphatemia, hypocalcemia, and hyperkalemia due to ingestion of phosphoric acid. Examination revealed ulcerative and hemorrhagic coagulation necrosis of the upper portions of the digestive tract. Caustic lesions were found in the gastric and intestinal mucosa; however, the esophagus was protected presumably due to its alkalinity and the speed the liquid passed through. Furthermore, regarding the respiratory system, the phosphoric acid provoked glottis edema; mucosal necrosis of the pharynx, hypopharynx, and trachea; and increased pulmonary edema. The patient developed depression of the central nervous system and a fatal cardiac dysrhythmia due to the electrolyte abnormalities. The dysrhythmia was in part due to hyperkalemia, which can also cause depolarization of cell membranes and inexcitability of cells to a development of lethal dysrhythmias including ventricular fibrillation. In conclusion, not only did the ingestion of acid produced local gastro-intestinal and respiratory mucosa, but it also caused systemic effects such as metabolic acidosis, hypophosphatemia, hypocalcemia and hyperkalemia and eventually death.
.
SUICIDE CASE DUE TO PHOSPHORIC ACID INGESTION
1667
References 1. Lupa M, Magne L, Lindhe Guarisco J, Amedee R. Update on the diagnosis and treatment of caustic ingestion. Ochsner J 2009;9:54–9. 2. Bureau of Policy and Strategy, Ministry of Public Health. Health statistic. Thailand Health Profile 2001-2004; http://www.moph.go.th/ops/ health_48 (accessed July 12, 2013). 3. Watson WA, Litovitz TL, Rodgers GC Jr, Klein-Schwartz W, Reid N, Youniss J, et al. 2004 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med 2005;23:589–666. 4. Vijayanath V, Nagaraja RK, Raju GM, Anitha MR. Forensic issues in suicide due to acid ingestion in a case of major depressive disorder. Am J Forensic Med Pathol 2012;33(2):156–8. 5. Pace F, Antinori F, Repici A. What is new in esophageal injury (infection, drug-induced, caustic, stricture, perforation)? Curr Opin Gastroenterol 2009;25:372–9. 6. Ashcraft KW, Padula RT. The effect of dilute corrosive of the esophagus. Pediatrics 1974;53:226–32. 7. Haller JA Jr, Andrews HG, White JJ, Tamer MA, Cleveland WW. Pathophysiology and management of acute corrosive burns of the esophagus: results of treatment in 285 children. J Pediatr Surg 1971;6:578–84. 8. Caravati EM. Metabolic abnormalities associated with phosphoric acid ingestion. Ann Emerg Med 1987;16:904–6. 9. Hebert LA, Lemann J Jr, Petersen JR, Lennon EJ. Studies of the mechanism by which phosphate infusion lowers serum calcium concentration. J Clin Invest 1966;45:1886–94. 10. Friedman EM. Caustic Ingestion and foreign bodies in the aerodigestive tract of children. Pediatr Clin North Am 1989;36(6):1403–10. 11. Slatopolsky E, Rutherford WE, Rosenbaum R, Martin K, Hruska K. Hyperphosphatemia. Clin Nephrol 1977;7:138–46. 12. Tanaka T, Tanaka N, Kita T, Kasai K, Sato HJ. Acephate in biological fluids of two autopsy cases after ingestion of the chemical. J Forensic Sci 2005;50(4):933–6. 13. Kamenczak A, Jasinska-Kolawa K, Targosz D, Szkolnicka B, Sancewicz-Pach K. Acute pesticides poisoning in the Krakow Department of Clinical Toxicology in 1986-1995. Przegl Lek 1997;54(10):671–6. 14. Aardema H, Meertens JH, Ligtenberg JJ, Peters-Polman OM, Tulleken JE, Zijlstra JG. Organophosphorus pesticide poisoning: cases and developments. Neth J Med 2008;66(4):149–53. 15. Harlak A, Yigit T, Coskun K, Ozer T, Mentes O, G€ulec B, et al. Surgical treatment of caustic esophageal strictures in adults. Int J Surg 2013;11(2):164–8. 16. Chirica M, Resche-Rigon M, Bongrand NM, Zohar S, Halimi B, Gornet JM, et al. Surgery for caustic injuries of the upper gastrointestinal tract. Ann Surg 2012;256(6):994–1001. 17. Cakal B, Akbal E, K€okl€u S, Babalı A, Kocßak E, Tasß A. Acute therapy with intravenous omeprazole on caustic esophageal injury: a prospective case series. Dis Esophagus 2013;26(1):22–6. Additional information and reprint requests: Isabella Aquila, M.D. Chair of Legal Medicine University Magna Graecia of Catanzaro Viale Europa loc. Germaneto 88100 Catanzaro Italy E-mail: [email protected]
