[Clinical analysis of 5 cases of acute poisoning by inhalation of hydrochlogen chloride].

Objective: To analyze the clinical characteristics caused by acute poisoning by inhalation of hydrogen chloride (HCl) and to raise awareness and treatment level of the disease. Methods: The clinical manifestations, imaging features, diagnosis, treatment and prognosis of 5 patients with acute HCl poisoning were analyzed retrospectively. Results: Among the 5 cases of HCl poisoning, 2 cases were severe poisoning, 3 cases were moderate poisoning. All patients were treated with corticosteroids and symptomatic treatment, one of them was treated with venovenous extracorporeal membrane oxygenation (VV-ECMO) . All patients were recovered and discharged from hospital. Conclusion: The lung damage of acute poisoning by inhalation of HCl is rapidly progressing, early detection and timely medical treatment can obtain a better prognosis.

An unusual presentation of hydrochloric acid ingestion: a mystery unraveled.

BACKGROUND: Unintentional acid ingestion is less commonly encountered than alkali ingestion. The injury develops for hours to days after ingestion and often results in progressively increasing difficulty in airway management. However, gastric perforation is rare. CASE: A 3-year-old boy presented to us with an orotonsillopharyngeal membrane and severe upper airway obstruction. Subsequently, he was diagnosed with a case of gastric perforation due to unintentional hydrochloric acid ingestion. He was treated with partial gastrectomy and feeding jejunostomy, and the recovery was good. CONCLUSIONS: Unintentional hydrochloric acid ingestion is rare in children. The manifestations masquerade many other clinical conditions, and the diagnosis is difficult in cases in which history of ingestion is not available. Treatment is symptomatic, and emergency surgery is indicated in case of gastrointestinal perforation.

Dispersion of acid without gastric perforation on ingestion of toilet cleaner: a rare autopsy case.

Toilet cleaner containing hydrochloric acid is a common item found in households all over the world. Due to the availability of the substance, it becomes one of the main contributors to corrosive damage to the gastrointestinal system. This study reports a case of a female in her 50s with an alleged history of ingestion of toilet cleaner an empty bottle of which was found together with a suicide note at the incident site. During the autopsy, the forensic expert made an intriguing observation regarding the dispersion of ingested acid to other organs without gastric perforation. Despite the absence of gastric perforation, the corrosive effects of the ingested acid were evident in various organs, including the liver and spleen. This phenomenon suggests a unique mechanism by which the acid is able to disperse and cause damage beyond the stomach, leading to widespread organ involvement. However, through a comprehensive analysis of the detailed history, typical macroscopic autopsy findings, and chemical analysis reports, it is possible to establish that the cause of death is corrosive acid poisoning. In such cases, further investigation is warranted to gain a better understanding of the underlying mechanisms responsible for the dispersion of the acid and its clinical implications. By delving deeper into these aspects, we can enhance our knowledge and contribute to the field of forensic medicine.

[The changes of peripheral blood lymphocyte subsets in patients with acute hydrogen chloride gas poisoning].

OBJECTIVE: To explore the changes of peripheral blood lymphocyte subsets in patients with acute hydrogen chloride gas poisoning. METHODS: When the patients were admitted or on the secondary day, the percentages of total T-cell lymphocyte subsets (CD(3)(+)CD(19)(-)), CD(4)(+)T cells (CD(3)(+)CD(4)(+)), CD(8)(+)T cells (CD(3)(+)CD(8)(+)), B cells (CD(3)(-)CD(19)(+)) and NK cells (CD(3)(-)CD(16)(+)CD(56)(+)), and the ration of CD(4)(+)/CD(8)(+) in 37 cases with acute hydrogen chloride gas poisoning and 49 healthy controls were detected with flow cytometer. RESULTS: The total T-cell percentage and total CD(4)(+)T cell percentage in 37 cases were significantly lower than those in 47 controls (P < 0.05). The percentages of NK cells and B lymphocytes in 37 cases significantly increased, as compared with controls (P < 0.05). The ration of CD(4)(+)/CD(8)(+) in 37 cases significantly decreased, as compared with controls (P < 0.05). CONCLUSION: The lymphocyte subsets in the patients with acute hydrogen chloride gas poisoning changed, which could influence the immune function of patients.

ARDS following inhalation of hydrochloric acid.

The clinical spectrum of Inhalation injury can range from mild cough to a devastating ARDS. We herewith present a patient who is a goldsmith by occupation and his work consists of dissolving gold in Hydrochloric acid. He had accidentally inhaled fumes of Hydrochloric acid and presented with cough and breathlessness, later on required mechanical ventilation for ARDS and improved. This highlights the importance of not to neglect mild symptoms like cough and dyspnea in such a scenario which may have some hidden catastrophe.

Bilateral ureteral obstruction from papillary necrosis secondary to household cleaner ingestion.

We report a case of a patient who developed bilateral hydroureteronephrosis from papillary necrosis secondary to ingestion of commercial toilet bowl cleaner. Eight days after her ingestion, acute renal failure prompted a renal ultrasound that showed bilateral hydroureteronephrosis. Emergent bilateral percutaneous nephrostomy tubes were placed and subsequent ureteroscopy revealed a large amount of obstructing necrotic material consistent with papillary necrosis. Ureteroscopic removal of the material and bilateral ureteral stents improved renal function. The etiology of this patient's papillary necrosis was likely due to a combination of hypovolemia, systemic acidosis from the ingestion, and direct toxicity of the substance on the renal vasculature. This case demonstrates the importance of early recognition of renal insults and the extra intestinal manifestations of toxic household ingestions.

Gastric tube interposition for corrosive esophagitis associated with pyloric stenosis.

Corrosive esophagitis, caused by swallowing corrosive acid or alkali, results in cicatricial stricture of the esophagus. The stricture is often accompanied by pyloric stenosis because strong acids act synergistically with gastric juice. Resection of both the esophagus and stomach is usually necessary, and the colon or jejunum is used as an esophageal substitute. We describe how we successfully treated corrosive esophagitis associated with pyloric stenosis, by performing gastric tube interposition for the esophageal reconstruction. After resecting the injured distal part of the stomach, we pulled the pedunculated gastric tube up to the cervix after anastomosis to the jejunal limb in a Roux-en-Y fashion. This reconstruction procedure prevented excessive organ sacrifice and was minimally invasive. Thus, esophageal reconstruction by interposition using a pedunculated gastric tube can be used effectively to treat corrosive esophagitis associated with pyloric stenosis.

Successful treatment of gastric necrosis after ingestion of hydrochloric acid: a two-stage minimally invasive surgical procedure.

Caustic ingestion may cause devastating injuries of the upper gastrointestinal tract and the respiratory system. We report here the successful treatment of a 37-year-old patient who ingested hydrochloric acid (100 mL; 24%) in suicidal intention. An oesophagogastroduodenoscopy revealed extensive necrosis of the gastric mucosa. A diagnostic laparoscopy was performed and confirmed the suspected transmural necrosis which resulted in a discontinuous laparoscopic gastrectomy. During the next days, the oesophageal stump was monitored through frequent oesophagoscopies and showed a good recovery. Thus, it was possible to restore continuity as early as by the sixth postoperative day performing a roux-en-y oesophagojejunostomy using the da Vinci Xi surgical robot. The patient underwent all procedures without any surgical complications and was discharged almost 1 month after initial presentation in good general condition.

Fatal myocardial infarction after hydrochloric acid ingestion in a suicide attempt.

Ingestion of acid-containing household products either accidentally or for suicide attempt is a common form of intoxication. Hydrochloric acid is widely used as an antirust compound or cleaner in homes and is highly corrosive and generally causes coagulation necrosis which could lead to perforation in the gastrointestinal system. Although hydrochloric acid ingestion is mainly harmful to the gastrointestinal system, it may also cause metabolic acidosis, hemolysis, renal failure, and fatality as well. Cardiovascular manifestations of hydrochloric acid ingestion are extremely rare, and we report a 48-year-old man who died of acute inferolateral myocardial infarction after hydrochloric acid ingestion in a suicide attempt who had no history of coronary artery disease. In conclusion, although cardiovascular manifestations of hydrochloric acid ingestion are extremely rare, the ingestion may still cause myocardial infarction which could be fatal. Physicians dealing with hydrochloric acid ingestion in the ED should be aware of this possibility and always obtain serial electrocardiograms even if the patient has no cardiac complaint.

ST segment elevation associated with hydrochloric acid ingestion: A case report.

RATIONALE: Electrocardiography (ECG) was used to diagnose acute coronary syndrome, but many other diseases may also result in ST segment change. We report one case of ingested hydrochloric acid present with ST segment elevation in the ECG. However, subsequent coronary angiography did not reveal significant coronary occlusion. PATIENT CONCERNS: An 83-year-old female was transferred to our emergency department (ED) from the branch hospital due to ingestion of toilet bowl cleaner containing 9.5% hydrochloric acid. She complained about chest pain and 12-lead ECG showed ST segment elevation at lead II, III, and aVF. The blood examinations revealed elevation of aspartate transaminase (69 IU/L), thrombocytopenia (62,000/µL), and acidosis (pH 7.311, pCO2 27 mm Hg, HCO3 13.3 mmol/L). Creatine kinase-MB and troponin I did not elevate then. DIAGNOSES: After transferred to our ED, coronary angiography was done within 1 hour. Angiography showed 60% stenosis in the segment 7 of left anterior descending coronary artery and 30% nonsignificant stenosis in the segment 2 of right coronary artery, with no apical ballooning. No significant lesion consistent with ST segment elevation myocardial infarction was found. INTERVENTIONS: Conservative treatment was chosen. OUTCOMES: Bradycardia was followed by cardiac arrest that developed 4 hours later. Cardiopulmonary resuscitation was applied and the patient became shock status after return of spontaneous circulation. The patient was admitted to the intensive care unit and expired on next day. LESSONS: Patients of ingested hydrochloric acid present with ST segment elevation in the ECG may not indicate coronary artery disease. This ECG finding may be a poor prognostic index in such patients.

Planned complex suicide: report of three cases.

This article presents three planned complex suicide cases. The first case was a 46-year-old man, who had taken some antidepressant and antipsychotic drugs before cutting his right wrist and ingesting a large amount of concentrated hydrochloric acid. In the second case, a 34-year-old man was found dead in his home, hanging by his neck, with a suicidal stab wound on the left side of the chest. In the third case, a 22-year-old woman was found dead, hanging by her neck from a ceiling beam of her grandmother's a storage room, after taking of a solid rodenticide. The histories revealed psychiatric problems in all cases. The investigation of scene, the method employed, the autopsy findings and the interview with their relatives altogether pointed toward a suicidal etiology.

Distribution of orally ingested hydrochloric acid in the thoracoabdominal cavity after death.

The authors encountered a case of hydrochloric acid (HCl) poisoning, thought to be caused by oral ingestion of concentrated HCl. Coagulation of the surface of the tongue and the mucosa of the pharynx, esophagus, and stomach were observed at forensic autopsy. An overabundance of Cl- was found in the gastric contents, corresponding to 8.19 mL of concentrated HCl. This was suggested to be a lethal oral dose of concentrated HCl, and the cause of death was determined to be HCl poisoning. Measuring the pH and concentrations of various ions in body fluids and contents of the alimentary tract enabled postmortem diffusion of HCl to be determined.

Acute myocardial infarction after hydrochloric acid ingestion.

We report a case of acute ST segment elevated myocardial infarction associated with hydrochloric acid ingestion. Severe systemic acidosis developed shortly after massive hydrochloric ingestion; it was complicated by the presence of acute myocardial infarction. A new complication of acid ingestion is presented and a possible mechanism is discussed.

Physiological and toxicological aspects of smoke produced during the combustion of polymeric materials.

Normally one expects that flame contact is the major cause of injury and death during fires. Analysis of the factors involved in numerous fires has revealed that most deaths were not due to flame contact, but were a consequence of the production of carbon monoxide, nitrogen oxides, and other combustion products, such as aldehydes, low molecular weight alcohols, hydrogen cyanide, and other noxious species. The major emphasis within the scope of this paper relates to the physiological and toxicological aspects of smoke produced during the combustion of materials. Special emphasis is directed toward laboratory procedures which have been developed to determine the qualitative and quantitative analysis of smoke, factors pertaining to smoke development, and to measure the response of laboratory animals exposed to smoke. The effects that fire retardants, incorporated into polymeric materials as a means of improving flammability characteristics, may have on smoke development, the mechanism of polymer degradation, and on the survival response of laboratory animals are also considered.

Poisoning caused by inhalation of hydrogen chloride, phosphorus oxychloride, phosphorus pentachloride, oxalyl chloride, and oxalic acid.

Eleven people accidentally inhaled a significant amount of a gaseous mixture of hydrogen chloride, phosphorus oxychloride, phosphorus pentachloride, oxalyl chloride, and oxalic acid. Clinical observations and laboratory tests were recorded from the time of admission throughout hospitalization. The main abnormalities were found in the respiratory tract and consisted of clinical and physiologic evidence of obstruction of the airways, mild interstitial and alveolar edema, a defect in diffusion, and inequalities of ventilation and perfusion that produced hypoxemia. All of these cleared within a short time.

Tracheobronchial stenosis from acid aspiration presenting as asthma.

We report a case of a 42-year-old man who fell in a vat of hydrochloric acid, resulting in ingestion and aspiration of acid. Initially, he suffered from a chemical pneumonitis and GI burns. He was released from the hospital without complications, only to return with signs and symptoms consistent with asthma. Evaluation revealed multiple areas of large airway stenosis, resulting from the chemical burns. The stenoses were treated with multiple stents.

Upper gastrointestinal tract ablation for patients with extensive injury after ingestion of strong acid.

OBJECTIVE: Extensive corrosive injury involving the structures beyond the pylorus caused by ingestion of strong acid has a poor prognosis. We reviewed six cases of patients who underwent total upper gastrointestinal tract ablation to see the effect of this extensive procedure for such an injury. DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: Six patients who ingested more than 250 mL of 20N hydrochloric acid were treated in the Department of Surgery, Chang Gung Memorial Hospital, Taipei, Taiwan, Republic of China, from 1986 to 1992. RESULTS: Three patients with preoperative metabolic acidosis and renal failure died of multiple organ failure within the first postoperative month. The other three patients survived the acute stage. While being readied for a late reconstructive procedure, sepsis developed in one patient due to cholecystostomy leakage about 1 year postoperatively. Another patient died of respiratory failure after development of aspiration pneumonia due to poor drainage of a spit fistula, after surviving for 6 months. Only one patient had a good recovery following a full reconstruction procedure and restoration of the continuity of the gastrointestinal tract. CONCLUSIONS: Three of six patients died in the hospital. The risk factors were preoperative metabolic acidosis, renal failure, and an upper jejunal resection greater than 100 cm in length. Early and aggressive approaches to resect all the necrotic tissue certainly provide good chances to survive the acute stage and later reconstruction.