Fatal multiple organ failure and disseminated intravascular coagulation in acute chromated copper arsenate poisoning

To the Editor:

Chromated copper arsenate (CCA) is widely used as a wood preservative, and chronic contamination and intoxication have been reported previously;^1–2 however, there are only two published cases of acute oral CCA poisoning.^3,4 One reported case focused on the distribution of the heavy metals in different body tissues based on postmortem analysis, with no description of the clinical manifestations, laboratory findings, or treatments.³ Another case survived for only 2.5 h after poisoning, so little information was available concerning the characteristics of organ injury and blood chemistry.⁴ Here, we describe a fatal case of acute oral CCA poisoning to provide more information on the clinical course and toxicological features following oral CCA ingestion.

A previously healthy, 60-year-old man was transported to our hospital and received a thorough gastric lavage 15 min after accidentally drinking approximately 10 mL of pure CCA (known as type C, composed of 47.5% Cr (VI) as CrO₃; 18.5% Cu (II) as CuO; and 34.0% As (V) as As₂O₅). On admission, the patient complained of nausea and abdominal distention, and experienced three episodes of watery diarrhea. His vital signs were as follows: T 36.5°C; BP 116/72 mm Hg; HR 134 beats per minute; RR 24 breaths per minute; and SpO₂ 98%. He was awake and alert, with no neuropsychiatric abnormalities. Physical examination was unremarkable apart from minor burns of the oropharyngeal mucosa and abdominal distension. Blood sample was collected and sent for heavy metal detection with results expected 12 h later. Blood test results 30 min post-ingestion were within normal limits for complete blood count; hepatic and renal function; myocardial enzymes; arterial blood gas; and coagulation profiles (Table 1). Urinalysis was not performed because of anuria. Routine examination of stool specimens was negative and an ECG showed a sinus tachycardia. Ultrasonography revealed diffuse parenchymal lesions of the liver and kidney, and pulmonary CT scan was unremarkable.

Table 1. Major laboratory parameters at various time-points following ingestion.

	30 min	10 h	24 h	30 h
WBC (× 10^9/L)	6.36	15.9	16.9	15.46
PLT (× 10^9/L)	122	85	34	26
ALB (g/L)	44.6	34.7	28.4	22.2
ALT (IU/L)	32	56	607	806
AST(IU/L)	34	104	901	1076
TBIL (umol/L)	15.3	50.6	113.1	112.6
Crea (mg/dL)	0.94	3.01	4.80	4.76
CK (IU/L)	158	299	1626	1297
LDH (IU/L)	238	393	1760	2011
pH	7.36	7.3	7.25	7.19
PaO2 (mmHg)	92	74	42	40
HCO3^− (mmol/L)	17.5	12.9	15.2	10.6
PT(s)	13.7	15	30.3	37.9
INR	1.2	1.23	2.9	3.68
APTT(s)	25.5	26.7	64.7	102.5
FIB(g/L)	2.6	1.84	1.32	0.84
TT(s)	16	19.3	27	32.3
D-dimer(mg/L)	2.7	25.2	21.98	19.48

Six hours after poisoning, the patient's blood pressure dropped and remained below 90/60 mm Hg. Scleral icterus developed gradually and the patient remained anuria throughout his hospitalization. The concentrations of heavy metals in the blood sample were reported 12 h after ingestion as follows: chromium (Cr) 300 mcg/L (reference range, 0.3–1.2 mcg/L), arsenic (As) 240 mcg/L (reference range, 0–5.1 mcg/L), and copper (Cu) 0.49 mg/L (reference range, 0–50 mg/L). Petechial hemorrhages, epistaxis, and bleeding from insertion sites of venous were noted 24 h after poisoning. As shown in Table 1, serial blood tests performed at 10, 24, and 30 h after poisoning indicated multiple organ failure (MOF) including leukocytosis, thrombocytopenia, acute liver injury and renal failure, myocardial injury, severe metabolic acidosis, and disseminated intravascular coagulation (DIC). Despite supportive care including fluid resuscitation, multiple vasopressors, bicarbonate, diuretics, and hepatic protectants, the patient's clinical status deteriorated and he expired 32 h after poisoning. Autopsy was refused by the family due to traditional beliefs.

In this case, abdominal distention, jaundice, refractory hypotension, and anuria were the most pronounced symptoms and signs, occurring within 6 h of ingestion. Refractory hypotension, burns of oropharyngeal mucosa, diarrhea, metabolic acidosis, and death occurred in both our case and a case reported by Hay et al.,⁴ which suggested the corrosive and fatal nature of CCA. However, the clinical manifestations were somewhat different between the two cases. Our case was characterized by MOF involving the hepatic, renal, hematological, and cardiovascular systems and DIC, but Hay et al.'s case developed severe respiratory distress, refractory arrhythmias, and circulatory failure, with death occurring 2.5 h after poisoning. The heavy metal blood analysis in our case indicated excessive Cr and As concentrations, but normal Cu concentration, consistent with previous reports.³ However, chelating agents such as dimercaprol (BAL) and dimercaptosuccinic acid (DMSA) were not administered because of anuria.

Acute exposure to high concentrations of CCA is rarely reported after oral ingestion, but usually occurs through inhalation of CCA-rich ashes, vapor, and air following burning of CCA-treated wood in an enclosed space. The metal concentrations (Cr plus Cu plus As) could be as high as 36% of the ash⁵, and 9–22% of the As was released in smoke when burning CCA-treated wood.⁶ Inhalation of CCA can cause multiple health problems involving the respiratory and circulatory systems, and the gastrointestinal tract. Severe hepatic and renal injuries, metabolic acidosis, and DIC are less common. Additionally, in previous reports, many symptoms gradually improved with treatment.^6,7 The different outcomes with oral vs. inhalational poisoning may be due to the different exposure and intake of CCA, with oral ingestion resulting in much higher levels than that through inhalation.

In summary, our case and previous cases reported by Cross et al.³ and Hay et al.⁴ indicated that ingestion of CCA solutions may result in fatal outcome, which can be accompanied by various clinical manifestations. Although most countries have restricted the use of CCA for residential construction, we emphasize the risk of acute oral CCA poisoning because CCA is still permitted for a wide variety of industrial and agricultural applications.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.