What are the causes and symptoms of gas vomiting. How is gastric emphysema diagnosed and treated. What is the significance of hepatoportal venous gas. When is conservative management appropriate for gastric pneumatosis.

Understanding Gas Vomiting and Gastric Pneumatosis

Gas vomiting is a condition characterized by excessive belching, nausea, and vomiting that may be accompanied by abdominal discomfort. In severe cases, it can lead to a rare condition called gastric pneumatosis, which refers to the presence of air within the wall of the stomach. Gastric pneumatosis encompasses two distinct entities: gastric emphysema (GE) and emphysematous gastritis.

Gastric emphysema is generally considered a benign condition that can result from various iatrogenic and non-iatrogenic causes. On the other hand, emphysematous gastritis is a more severe and potentially life-threatening condition associated with infection and inflammation of the stomach wall.

What causes gastric emphysema?

• Recurrent vomiting and retching
• Gastric outlet obstruction
• Excessive air swallowing (aerophagia)
• Gastric surgery or endoscopic procedures
• Caustic ingestion
• Blunt abdominal trauma

The Link Between Gastric Emphysema and Hepatoportal Venous Gas

In some cases of gastric emphysema, air within the stomach wall can dissect through tissue planes and enter the portal venous system, leading to hepatoportal venous gas (HPVG). Historically, HPVG was considered an ominous radiological sign indicative of severe abdominal pathology, often necessitating emergency surgical intervention.

However, with the increasing use of advanced imaging techniques, particularly CT scans, a growing number of benign cases of HPVG have been identified. These cases can often be managed conservatively without the need for invasive surgical procedures.

What are the potential causes of hepatoportal venous gas?

• Intestinal ischemia or necrosis
• Bowel obstruction
• Inflammatory bowel disease
• Intra-abdominal sepsis
• Gastric dilatation
• Iatrogenic causes (e.g., endoscopic procedures)

Clinical Presentation and Diagnosis of Gastric Emphysema

Patients with gastric emphysema may present with a range of symptoms, from mild discomfort to severe abdominal pain. Common clinical features include:

• Epigastric pain or discomfort
• Nausea and vomiting
• Abdominal distension
• Excessive belching
• Fever (in cases of emphysematous gastritis)

Diagnosis of gastric emphysema and associated HPVG primarily relies on imaging studies. CT scan is the gold standard for diagnosis, offering high sensitivity and specificity in detecting air within the gastric wall and portal venous system.

How does CT imaging aid in the diagnosis of gastric emphysema?

CT scans can reveal the presence of air within the gastric wall, appearing as a characteristic linear or curved lucency. In cases of HPVG, branching radiolucencies in the peripheral regions of the liver can be observed, typically extending to within 2 cm of the liver capsule.

Management Strategies for Gastric Emphysema and HPVG

The management of gastric emphysema and HPVG depends on the underlying cause and the patient’s clinical condition. In many cases, especially those related to benign causes such as vomiting or iatrogenic procedures, conservative management can be appropriate and effective.

What does conservative management entail?

• Bowel rest and nasogastric decompression
• Intravenous fluid resuscitation
• Antiemetic medications
• Proton pump inhibitors or H2 receptor antagonists
• Close monitoring of vital signs and laboratory parameters
• Serial imaging to assess resolution of pneumatosis

In cases where there is suspicion of intestinal ischemia, bowel necrosis, or other life-threatening conditions, surgical intervention may be necessary. The decision between conservative and surgical management should be based on a thorough clinical assessment, laboratory findings, and imaging results.

The Role of Endoscopy in Gastric Emphysema

While CT imaging is the primary diagnostic tool for gastric emphysema and HPVG, endoscopy can play a valuable role in certain cases. Endoscopic evaluation can help assess the extent of mucosal damage, identify potential underlying causes, and guide treatment decisions.

When is endoscopy indicated in cases of gastric emphysema?

• To rule out gastric ischemia or necrosis
• To evaluate for gastric outlet obstruction
• To assess for mucosal lesions or ulcerations
• To obtain biopsies in cases of suspected emphysematous gastritis

However, it’s important to note that in some cases, endoscopy may be contraindicated due to the risk of perforation or exacerbation of pneumatosis. The decision to perform endoscopy should be made on a case-by-case basis, weighing the potential benefits against the risks.

Prognosis and Follow-up for Gastric Emphysema Patients

The prognosis for patients with gastric emphysema largely depends on the underlying cause and the presence of associated complications. In cases of benign gastric emphysema, such as those induced by vomiting or iatrogenic causes, the prognosis is generally favorable with appropriate conservative management.

What factors influence the prognosis of gastric emphysema?

• Underlying cause (benign vs. life-threatening)
• Presence of associated complications (e.g., perforation, ischemia)
• Timeliness of diagnosis and initiation of treatment
• Patient’s overall health status and comorbidities

Follow-up care for patients with gastric emphysema typically involves repeat imaging to ensure resolution of pneumatosis and HPVG. The frequency and duration of follow-up depend on the severity of the initial presentation and the patient’s clinical course.

Differential Diagnosis: Gastric Emphysema vs. Emphysematous Gastritis

While gastric emphysema and emphysematous gastritis can present with similar radiological findings, they are distinct entities with different pathophysiologies and clinical implications. Distinguishing between these two conditions is crucial for appropriate management and prognosis.

How do gastric emphysema and emphysematous gastritis differ?

Emphysematous gastritis is a more severe condition associated with infection by gas-forming organisms. It requires prompt recognition and aggressive management, often including broad-spectrum antibiotics and sometimes surgical intervention.

Preventing Recurrence of Gastric Emphysema

While not all cases of gastric emphysema are preventable, certain measures can be taken to reduce the risk of recurrence, particularly in cases related to vomiting or gastric distension.

What strategies can help prevent recurrent gastric emphysema?

• Identifying and treating underlying gastrointestinal disorders
• Managing conditions that predispose to frequent vomiting
• Avoiding excessive air swallowing during eating and drinking
• Proper technique during nasogastric tube placement and gastric decompression
• Careful monitoring during endoscopic procedures

Patient education plays a crucial role in prevention. Individuals with a history of gastric emphysema should be informed about the potential triggers and warning signs to watch for. They should be encouraged to seek prompt medical attention if symptoms recur.

Emerging Research and Future Directions

As our understanding of gastric emphysema and hepatoportal venous gas continues to evolve, ongoing research aims to refine diagnostic criteria, improve risk stratification, and optimize management strategies.

What are some areas of active research in gastric emphysema?

• Development of predictive models for identifying high-risk patients
• Exploration of novel imaging techniques for early detection
• Investigation of the microbiome’s role in emphysematous gastritis
• Evaluation of minimally invasive interventions for complicated cases

Future studies may focus on elucidating the exact pathophysiological mechanisms underlying gastric emphysema and HPVG, which could lead to more targeted therapeutic approaches. Additionally, long-term follow-up studies of patients with benign gastric emphysema may provide valuable insights into the natural history and potential long-term consequences of this condition.

In conclusion, gastric emphysema and hepatoportal venous gas represent a spectrum of conditions ranging from benign to life-threatening. Advances in imaging technology have improved our ability to diagnose these entities and have revealed that many cases can be managed conservatively. However, careful clinical assessment and appropriate use of diagnostic tools remain crucial for distinguishing between benign and potentially catastrophic causes. As research in this field progresses, we can anticipate further refinements in diagnostic and management strategies, ultimately leading to improved outcomes for patients with these rare but significant conditions.

Vomiting-Induced Gastric Emphysema and Hepatoportal Venous Gas: A Case Report and Review of the Literature

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Case Rep Med. 2015; 2015: 413230.

Published online 2015 Feb 11. doi: 10.1155/2015/413230

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Gastric pneumatosis is the presence of air within the wall of the stomach. It represents a spectrum of conditions ranging from benign disease to septic shock and death. Etiopathologically, it can be classified into emphysematous gastritis or gastric emphysema (GE). Along with hepatoportal venous gas (HPVG), it was considered as an ominous radiological sign and warranted an emergent surgical exploration; however, with widespread use of computerized tomographic (CT) scan, an increasing number of benign causes of GE and HPVG have been reported in the literature, where patients can be managed by noninvasive and conservative measures. We hereby describe a case where recurrent episodes of vomiting led to development of GE and HPVG and the patient was managed successfully by conservative measures.

Gastric pneumatosis refers to the presence of air within the wall of the stomach. It can be classified into two types: gastric emphysema (GE) and emphysematous gastritis. GE is essentially non-life threatening and can be caused by a variety of iatrogenic and noniatrogenic events [1–6]. Pulmonary, trauma, and obstruction are the three principal theories proposed to explain its pathogenesis. They have a benign clinical course and patients often have uneventful recovery with conservative treatment [1].

In rare instances, air within the stomach wall can dissect through the tissue planes and reach the portal veins, leading to hepatoportal venous gas (HPVG). Now from a radiological stand point HPVG denotes a catastrophic abdominal event like intestinal necrosis or bowel obstruction mandating urgent surgical intervention. However with growing use of CT scans in recent times, several benign cases of HPVG are described in the literature where invasive surgical approach is often not required and patients can be managed conservatively. CT scan plays an important role in such cases of acute abdomen to identify the underlying etiological process and help the clinician choose conservative over surgical treatment option [6–8]. We hereby present a case of GE and HPVG induced by vomiting where patient was successfully managed by conservative measures. Also presented is a review of the literature to shed a light on etiology, clinical presentation, and management strategies in cases of GE, emphysematous gastritis, and HPVG.

A 58-year-old male presented to the emergency room with complaints of abdominal pain, nausea, and multiple episodes of vomiting for last twenty-four hours. Patient described a sharp epigastric pain with 8–10 episodes of bilious vomiting and retching. He denied eating unusual food or taking over the counter pain medications. Patient had regular bowel movements and denied any blood in the stool. His past medical history included end stage renal disease requiring hemodialysis and peripheral vascular disease.

On physical examination, pulse was 90 beats per minute, blood pressure was 150/90 mm of Hg, and temperature was 98.6° F. Mild tenderness was present in the epigastric region, but abdomen was otherwise soft and without guarding or rigidity. Fecal occult blood test was negative. The remainder of the physical exam was unremarkable.

Patient had an elevated white blood cell (WBC) count to 13.4 k/mm³ (Normal range: 4–11 k/mm³). Lactic acid level was elevated to 2.7 mmol/L (normal range: 0.7–2.2 mmol/L). Serum amylase, serum lipase, and rest of the comprehensive metabolic panel were within normal limits. Subsequently, a computerized tomography (CT) scan of the abdomen was obtained which revealed air in the wall of the stomach along with large amount of air in the liver, spleen, portal vein, superior mesenteric vein, and splenic vein (). However, there was no intestinal obstruction, intra-abdominal free air, or free fluid. Surgery was consulted as gastric pneumatosis and portal venous gas raised the suspicion of intestinal ischemia and bowel necrosis.

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(a) Blue arrow showing air in the wall of the stomach. (b) Blue arrow showing air in the intrahepatic branches of portal vein. (c) Coronal section of the abdomen with upper arrow showing air in the intrahepatic branch of portal vein and lower arrow showing air in the area of confluence of portal vein. (d) Blue arrow showing air in the stomach wall and red arrow showing air in the spleen.

In spite of the worrisome findings on the CT scan, patient was hemodynamically stable and abdominal examination was completely benign. Therefore, he was treated conservatively with bowel rest, gastric decompression, intravenous fluids, and antibiotics. He improved significantly over the next 2 days. A repeat CT scan of the abdomen (obtained after 48 hours from presentation) showed complete resolution of gastric pneumatosis and portal venous air (). The proposed mechanism of these radiologic findings was that repeated episodes of vomiting and retching led to gastric emphysema in our patient, with subsequent dissection of air into the portal venous system. He was started on a clear liquid diet with gradual advancement. Antibiotics were discontinued and he was discharged home in stable condition.

Open in a separate window

Contrast enhanced CT scan of the abdomen (48 hours after presentation) showing resolution of gas in the wall of the stomach, portal veins, and spleen.

There are two types of gastric pneumatosis, emphysematous gastritis and gastric emphysema [1]. Emphysematous gastritis may occur by direct inoculation of gas-producing bacteria into the gastric mucosa or by hematogenous spread. Clostridium perfringens, Escherichia coli, Pseudomonas aeruginosa, Streptococci, Staphylococci, and Enterobacter species are the most frequent causative agents [9]. Immunosuppression, diabetes mellitus, ingestion of corrosive substances, alcoholism, and nonsteroidal anti-inflammatory drugs ingestion are common predisposing factors. Affected patients are very ill with severe abdominal pain, peritoneal signs, and elevated WBCs, often resulting in a fulminant clinical course, shock, and a high rate of mortality [9, 10].

Unlike emphysematous gastritis, GE is noninfectious in origin and occurs primarily due to entry of intraluminal air into the wall of the stomach. It may be divided into three etiological categories: traumatic, obstructive, and pulmonary [1].

Traumatic GE is caused by transmural diffusion of air after a mucosal injury, which can occur during esophagogastroduodenoscopy (EGD), severe vomiting, cardiopulmonary resuscitation (CPR), or acute gastric dilatation caused by eating disorders [2–4, 6, 11]. Obstructive GE has been reported in patients with gastric outlet obstruction due to a variety of conditions. The increase in the intragastric pressure accompanied by damaged gastric mucosa permits the entry of air into the wall of the stomach. Gastric carcinoma, gastric volvulus, duodenal obstruction, and hypertrophic pyloric stenosis in children have been reported as causes of obstructive GE [1, 5]. Pulmonary GE is caused by alveolar rupture and air leaks, which then track through the mediastinum and dissecting downwards to reach the stomach wall [1].

Clinical manifestations in GE are usually nonspecific. Patients may present with nausea, vomiting, epigastric discomfort, or abdominal pain. Importantly, patients are almost always hemodynamically stable and do not show signs of acute abdomen. In general, it has a benign clinical course and resolves spontaneously without any clinical sequel [1–4, 6].

HPVG was frequently seen with bowel necrosis, small bowel obstruction, peptic ulcer disease, and intra-abdominal abscess [7]. Hence presence of gas in the portal venous system was often considered to represent an intra-abdominal catastrophic event. However, with advances in imaging techniques and increasing availability of CT scans, many benign cases of HPVG have been found. Ulcerative colitis, barium enemas, colonoscopy, liver transplantation, GE, and cardiopulmonary resuscitation represent such benign causes of HPVG. Conservative treatment is successful in many of these cases without surgical intervention [7, 8, 12, 13].

Hussain et al. have classified patients into three broad groups to simplify the treatment approach. First, patients with HPVG and signs of acute abdomen are best treated with emergent surgery. Second, patients with HPVG who lack clinical signs and demonstrate stable hemodynamic parameters should receive conservative management. Finally, patients with HPVG and uncertain clinical features should undergo endoscopy and/or diagnostic laparoscopy to rule out underlying bowel ischemia [13].

We believe that, in our case, repeated episodes of vomiting and retching caused damage to the gastric mucosa and sudden increase in the intragastric pressure. This led to dissection and leaking of air into the intramural layer of the stomach wall and subsequent spread to the portal veins, superior mesenteric vein, and splenic vein (). Because the patient presented with benign physical exam and laboratory findings, a conservative treatment approach was chosen. Clinical improvement and spontaneous resolution of air within two days as confirmed by a repeat CT scan of the abdomen () further substantiated our theory that the etiology of visceral air was benign and not due to ischemia of the bowel or stomach. Hence, HPVG does not always indicate serious intra-abdominal pathology. It can be associated with benign conditions as described above. Also HPVG is just a radiological sign and it should not be solely relied upon in deciding between surgical intervention and conservative treatment; rather entire clinical picture including underlying etiology, clinical examination, and laboratory parameters should be taken into consideration [13, 14].

The presence of air in the wall of stomach may be due to GE, which is often self-resolving, or due to emphysematous gastritis, which heralds worse prognosis. Superimposed occurrence of air in the portal venous system often causes a dilemma when considering surgical options. Historically, presence of gas in the portal venous system was considered as an acute abdominal emergency and warranted urgent surgical intervention but recently many benign causes of GE and HPVG have been described in the literature. These new cases were not associated with serious abdominal pathology and did not require surgical intervention. Therefore, HPVG by itself should no longer be an indication for emergent surgical intervention.

The authors declare that there is no conflict of interests regarding the publication of this paper.

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Adamsite (DM): Vomiting Agent | NIOSH

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CAS #:

CAS #: 578-94-9

RTECS #: SG0680000

UN #: 1698 (Guide 154)

Common Names:

• 10-chloro-5,10-dihydroarsacridine
• 10-chloro-5,10-dihydrophenarsazine
• 5-aza-10-arsenaanthracene chloride
• Diphenylaminechlorarsine

Agent Characteristics

Light green to yellow crystals (solid) at room temperature. When dispersed by heat, fine particulate smoke; canary yellow when concentrated, colorless when diluted with air.

Adamsite (DM) is a vomiting compound that has been used as a riot-control agent (military designation, DM). It is released as an aerosol. Adverse health effects due to exposure to adamsite (DM) are generally self-limited and do not require specific therapy. Most adverse health effects resolve within 30 minutes. Exposure to large concentrations of adamsite (DM), or exposure to adamsite (DM) within an enclosed space or under adverse weather conditions, may result in more severe adverse health effects, serious illness, or death.

• Indoor Air: Adamsite (DM) can be released into indoor air as fine particles (aerosol).
• Water: Adamsite (DM) is not soluble in water and cannot be used to contaminate water.
• Food: Not established/determined
• Outdoor Air: Adamsite (DM) can be released into outdoor air as fine particles (aerosol).
• Agricultural: If adamsite (DM) is released into the air as fine particles (aerosol), it has the potential to contaminate agricultural products.

Adamsite (DM) can affect the body through inhalation, ingestion, skin contact, or eye contact. Ingestion is an uncommon route of exposure.

Personal Protective Equipment

First Responders should use a NIOSH-certified Chemical, Biological, Radiological, Nuclear (CBRN) Self Contained Breathing Apparatus (SCBA) with a Level A protective suit when entering an area with an unknown contaminant or when entering an area where the concentration of the contaminant is unknown. Level A protection should be used until monitoring results confirm the contaminant and the concentration of the contaminant.
NOTE: Safe use of protective clothing and equipment requires specific skills developed through training and experience.

Select when the greatest level of skin, respiratory, and eye protection is required. This is the maximum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than the AEGL-2.

• A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle.
• A Totally-Encapsulating Chemical Protective (TECP) suit that provides protection against CBRN agents.
• Chemical-resistant gloves (outer).
• Chemical-resistant gloves (inner).
• Chemical-resistant boots with a steel toe and shank.
• Coveralls, long underwear, and a hard hat worn under the TECP suit are optional items.

Select when the highest level of respiratory protection is necessary but a lesser level of skin protection is required. This is the minimum protection for workers in danger of exposure to unknown chemical hazards or levels above the IDLH or greater than AEGL-2. It differs from Level A in that it incorporates a non-encapsulating, splash-protective, chemical-resistant splash suit that provides Level A protection against liquids but is not airtight.

• A NIOSH-certified CBRN full-face-piece SCBA operated in a pressure-demand mode or a pressure-demand supplied air hose respirator with an auxiliary escape bottle.
• A hooded chemical-resistant suit that provides protection against CBRN agents.
• Chemical-resistant gloves (outer).
• Chemical-resistant gloves (inner).
• Chemical-resistant boots with a steel toe and shank.
• Coveralls, long underwear, a hard hat worn under the chemical-resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items.

Select when the contaminant and concentration of the contaminant are known and the respiratory protection criteria factors for using Air Purifying Respirators (APR) or Powered Air Purifying Respirators (PAPR) are met. This level is appropriate when decontaminating patient/victims.

• A NIOSH-certified CBRN tight-fitting APR with a canister-type gas mask or CBRN PAPR for air levels greater than AEGL-2.
• A NIOSH-certified CBRN PAPR with a loose-fitting face-piece, hood, or helmet and a filter or a combination organic vapor, acid gas, and particulate cartridge/filter combination or a continuous flow respirator for air levels greater than AEGL-1.
• A hooded chemical-resistant suit that provides protection against CBRN agents.
• Chemical-resistant gloves (outer).
• Chemical-resistant gloves (inner).
• Chemical-resistant boots with a steel toe and shank.
• Escape mask, face shield, coveralls, long underwear, a hard hat worn under the chemical-resistant suit, and chemical-resistant disposable boot-covers worn over the chemical-resistant suit are optional items.

Select when the contaminant and concentration of the contaminant are known and the concentration is below the appropriate occupational exposure limit or less than AEGL-1 for the stated duration times.

• Limited to coveralls or other work clothes, boots, and gloves.

Emergency Response

• Adamsite (DM) corrodes iron, bronze, and brass.
• Contact with metals may evolve flammable hydrogen gas.

• Containers may explode when heated.

• Adamsite (DM) is non-combustible.
• The agent itself does not burn, but it may decompose upon heating to produce corrosive and/or toxic fumes.
• Fire may produce irritating, corrosive, and/or toxic gases.
• The agent may be an oxidant, and it may ignite combustibles (wood, paper, oil, clothing, etc.).
• For small fires, use dry chemical, carbon dioxide, or water spray.
• For large fires, use dry chemical, carbon dioxide, alcohol-resistant foam, or water spray. Move containers from the fire area if it is possible to do so without risk to personnel. Dike fire control water for later disposal; do not scatter the material.
• For fire involving tanks or car/trailer loads, fight the fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after the fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tanks. Always stay away from tanks engulfed in fire.
• Run-off from fire control or dilution water may be corrosive and/or toxic, and it may cause pollution.
• If the situation allows, control and properly dispose of run-off (effluent).

• If a tank, rail car, or tank truck is involved in a fire, isolate it for 0.5 mi (800 m) in all directions; also consider initial evacuation for 0.5 mi (800 m) in all directions.
• Small spills (involving the release of approximately 52.83 gallons (200 liters) or less), when used as a weapon
• First isolate in all directions: 200 ft (60 m).
• Then protect persons downwind during the day: 0.2 mi (0.4 km).
• Then protect persons downwind during the night: 0.7 mi (1.2 km).
• Large spills (involving quantities greater than 52.83 gallons (200 liters)), when used as a weapon
• First isolate in all directions: 600 ft (180 m).
• Then protect persons downwind during the day: 1.4 mi (2.3 km).
• Then protect persons downwind during the night: 3. 2 mi (5.2 km).

• Aerosol may collect and stay in confined areas (e.g., sewers, basements, and tanks).
• Hazardous concentrations may develop quickly in enclosed, poorly-ventilated, or low-lying areas. Keep out of these areas. Stay upwind.

• Health: 2
• Flammability: 1
• Reactivity: 0
• Special:

• OSHA: Not established/determined
• NIOSH: Not established/determined

References are provided for the convenience of the reader and do not imply endorsement by NIOSH.

• AIR MATRIX
  No references were identified for this sampling matrix for this agent.
• OTHER
  Schoene K, Steinhanses J, Bruckert HJ, König A [1992]. Speciation of arsenic-containing chemical warfare agents by gas chromatographic analysis after derivatization with thioglycolic acid methyl ester. J Chromatogr A 605(2):257-262.
• SOIL MATRIX
  Haas R, Schmidt TC, Steinbach K, von Low E [1998]. Chromatographic determination of phenylarsenic compounds. Fresenius J Anal Chem 361(3):313-318.Schoene K, Bruckert HJ, Jürling H, Steinhanses J [1996]. Derivatization of 10-chloro-5,10-dihydrophenarsazine (Adamsite) for gas chromatographic analysis. J Chromatogr A 719(2):401-409.Vermeer H, Lourens R, Bickelhaupt F [1975]. An investigation of the structure of the so-called phenarsazine: Mass spectroscopical evidence for the thermal formation of phenarsazine. Tetrahedron 31(20):2529-2535.
• SURFACES
  No references were identified for this sampling matrix for this agent.
• WATER
  Haas R, Schmidt TC, Steinbach K, von Low E [1988]. Chromatographic determination of phenylarsenic compounds. Fresenius J Anal Chem 361(3):313-318.

Signs/Symptoms

The short-term effects of adamsite (DM) exposure begin 2 to 4 minutes after the onset of exposure. Prolonged whole-body (systemic) effects may last for 1 to 2 hours. Inhalation of DM in an outdoor environment results in adverse health effects that usually resolve in 20 minutes to 2 hours, leaving no residual effects. Inhalation of DM in an indoor environment may produce serious illness or death.

Exposure to adamsite (DM) causes rapid onset irritation of the eyes, upper airway, and skin and also nausea and vomiting (emesis). Whole-body (systemic) effects are more prolonged, lasting for several hours after exposure. If concentrations are low, initial symptoms may resemble those of a severe cold.

• Irritation and burning, tear production (lacrimation), spasmodic blinking (blepharospasm), swelling of the blood vessels that supply the membranes lining the eye (conjunctival injection), necrosis of the corneal epithelium.

• Not established/determined

• Short-term effects: Upper respiratory tract irritation in nose and sinuses, burning in throat, chest tightness and pain, uncontrollable and violent coughing and sneezing, greatly increased nasal secretions and oral secretions.
• Whole-body (systemic) effects: Nausea, vomiting (emesis), abdominal cramps, diarrhea, feeling of generalized weakness (malaise), headache, mental depression, and chills.

• Dermal exposures to low concentrations of adamsite (DM) are likely to produce short-lived skin redness (erythema) and irritation. Exposure to higher concentrations of adamsite (DM) can result in more severe, longer-lasting redness, itching, and swelling possibly followed by blister (vesicle) formation. More severe skin irritation may require symptomatic treatment.

Decontamination

The purpose of decontamination is to make an individual and/or their equipment safe by physically removing toxic substances quickly and effectively. Care should be taken during decontamination, because absorbed agent can be released from clothing and skin as a gas. Your Incident Commander will provide you with decontaminants specific for the agent released or the agent believed to have been released.

The following are recommendations to protect the first responders from the release area:

• Position the decontamination corridor upwind and uphill of the hot zone.
• The warm zone should include two decontamination corridors. One decontamination corridor is used to enter the warm zone and the other for exiting the warm zone into the cold zone. The decontamination zone for exiting should be upwind and uphill from the zone used to enter.
• Decontamination area workers should wear appropriate PPE. See the PPE section of this card for detailed information.
• A solution of detergent and water (which should have a pH value of at least 8 but should not exceed a pH value of 10.5) should be available for use in decontamination procedures. Soft brushes should be available to remove contamination from the PPE.
• Labeled, durable 6-mil polyethylene bags should be available for disposal of contaminated PPE.

The following methods can be used to decontaminate an individual:

• Decontamination of First Responder:
  • Begin washing PPE of the first responder using soap and water solution and a soft brush. Always move in a downward motion (from head to toe). Make sure to get into all areas, especially folds in the clothing. Wash and rinse (using cold or warm water) until the contaminant is thoroughly removed.
  • Remove PPE by rolling downward (from head to toe) and avoid pulling PPE off over the head. Remove the SCBA after other PPE has been removed.
  • Place all PPE in labeled durable 6-mil polyethylene bags.
• Decontamination of Patient/Victim:
  • Remove the patient/victim from the contaminated area and into the decontamination corridor.
  • Remove all clothing (at least down to their undergarments) and place the clothing in a labeled durable 6-mil polyethylene bag.
  • Thoroughly wash and rinse (using cold or warm water) the contaminated skin of the patient/victim using a soap and water solution. Be careful not to break the patient/victim’s skin during the decontamination process, and cover all open wounds.
  • Cover the patient/victim to prevent shock and loss of body heat.
  • Move the patient/victim to an area where emergency medical treatment can be provided.

First Aid

The effects of exposure to vomiting agents under usual outdoor conditions generally are self-limited, disappearing in 20 minutes to 2 hours, and require no specific therapy other than symptomatic relief. Exposure to large concentrations of adamsite (DM), or exposure to adamsite (DM) within an enclosed space or under adverse weather conditions, may result in more severe adverse health effects, serious illness, or death and may require supportive measures for symptomatic complaints of eye, skin, and airway irritation.

There is no antidote for adamsite (DM) toxicity.

• Immediately remove the patient/victim from the source of exposure.
• Immediately wash eyes with large amounts of tepid water for at least 15 minutes.
• Provide symptomatic relief.
• Seek medical attention immediately.

• Immediately remove the patient/victim from the source of exposure.
• Provide symptomatic relief.
• Seek medical attention immediately.

• Immediately remove the patient/victim from the source of exposure.
• Evaluate respiratory function and pulse.
• Ensure that the patient/victim has an unobstructed airway.
• If shortness of breath occurs or breathing is difficult (dyspnea), administer oxygen.
• Assist ventilation as required. Always use a barrier or bag-valve-mask device.
• If breathing has ceased (apnea), provide artificial respiration.
• Gargling may provide symptomatic relief.
• Seek medical attention immediately.

• Immediately remove the patient/victim from the source of exposure.
• May require the use of soothing compounds such as calamine, camphor, or mentholated creams.
• See the Decontamination section for patient/victim decontamination procedures.
• Seek medical attention immediately.

Long-Term Implications

A small minority (fewer than 1%) of people will experience serious, prolonged adverse health effects following adamsite exposure. Those seeking medical attention will generally have complaints relating to ocular, airway, and/or skin irritation. Patient/victims with severe or prolonged adverse health effects should be observed until effects abate.
Eyes should be carefully examined for retained foreign bodies and irrigated with water or saline. Use of topical antibiotics and eye solutions to relieve irritation should be used and referral to an ophthalmologist is suggested.
Use of oxygen and bronchodilators (if bronchospasm is present) may be necessary in patients with underlying respiratory disease.
More persistent and severe skin irritation may require the use of soothing compounds such as calamine, camphor, or mentholated creams. Large blisters, if present, should be debrided and irrigated several times daily. Use of a topical dermal antibiotic is recommended.

Not established/determined

Information is unavailable about the carcinogenicity, developmental toxicity, or reproductive toxicity of chronic or repeated exposure to adamsite (DM).

On-Site Fatalities

• Consult with the Incident Commander regarding the agent dispersed, dissemination method, level of PPE required, location, geographic complications (if any), and the approximate number of remains.
• Coordinate responsibilities and prepare to enter the scene as part of the evaluation team along with the FBI HazMat Technician, local law enforcement evidence technician, and other relevant personnel.
• Begin tracking remains using waterproof tags.

• Wear PPE until all remains are deemed free of contamination.
• Establish a preliminary (holding) morgue.
• Gather evidence, and place it in a clearly labeled impervious container. Hand any evidence over to the FBI.
• Remove and tag personal effects.
• Perform a thorough external evaluation and a preliminary identification check.
• See the Decontamination section for decontamination procedures.
• Decontaminate remains before they are removed from the incident site.

See Guidelines for Mass Fatality Management During Terrorist Incidents Involving Chemical Agents, U.S. Army Soldier and Biological Chemical Command (SBCCOM), November, 2001 for detailed recommendations.

Occupational Exposure Limits

• NIOSH REL:
  • Not established/determined
• OSHA PEL:
  • Not established/determined
• ACGIH TLV:
  • Not established/determined
• NIOSH IDLH: Not established/determined

• DOE TEEL:
  • TEEL-0: Not established/determined
  • TEEL-1: Not established/determined
  • TEEL-2: Not established/determined
  • TEEL-3: Not established/determined
• AIHA ERPG:
  • ERPG-1: Not established/determined
  • ERPG-2: Not established/determined
  • ERPG-3: Not established/determined

Acute Exposure Guidelines

Acute Exposure Guidelines [Interim]

	10 min	30 min	60 min	4 hr	8 hr
AEGL 1 (discomfort, non-disabling) – mg/m3	0. 20 mg/m3	0.041 mg/m3	0.016 mg/m3	0.0022 mg/m3	0.00083 mg/m3
AEGL 2 (irreversible or other serious, long-lasting effects or impaired ability to escape) – mg/m3	9.7 mg/m3	6.8 mg/m3	2.6 mg/m3	0.36 mg/m3	0.14 mg/m3
AEGL 3 (life-threatening effects or death) – mg/m3	21 mg/m3	17 mg/m3	6.4 mg/m3	0.91 mg/m3	0.34 mg/m3

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NOTE THAT VALUES ARE IN mg/m³, NOT ppm.

Technical Support Document

IMPORTANT NOTE: Interim AEGLs are established following review and consideration by the National Advisory Committee for AEGLs (NAC/AEGL) of public comments on Proposed AEGLs. Interim AEGLs are available for use by organizations while awaiting NRC/NAS peer review and publication of Final AEGLs. Changes to Interim values and Technical Support Documents may occur prior to publication of Final AEGL values. In some cases, revised Interim values may be posted on this Web site, but the revised Interim Technical Support Document for the chemical may be subject to change. (Further information is available through AEGL Process).

Decontamination (Environment and Equipment)

The following methods can be used to decontaminate the environment/spillage disposal:

• Do not touch or walk through the spilled agent if at all possible. However, if you must, personnel should wear the appropriate PPE during environmental decontamination. See the PPE section of this card for detailed information.
• Keep combustibles (e.g., wood, paper, and oil) away from the spilled agent.
• Use water spray to reduce vapors or divert vapor cloud drift. Avoid allowing water runoff to contact the spilled agent.
• Do not direct water at the spill or the source of the leak.
• Stop the leak if it is possible to do so without risk to personnel, and turn leaking containers so that gas rather than liquid escapes.
• Prevent entry into waterways, sewers, basements, or confined areas.
• Isolate the area until gas has dispersed.
• Ventilate the area.

Agents can seep into the crevices of equipment making it dangerous to handle. The following methods can be used to decontaminate equipment:

• Not established/determined

Agent Properties

• Chemical Formula:
  C₁₂H₉AsClN
• Aqueous solubility:
  Slightly soluble
• Boiling Point:
  770°F (410°C) (decomposes)
• Density:
  Solid: 1.65
  Vapor: Negligible
• Flammability:
  Not combustible
• Flashpoint:
  Does not flash

• Ionization potential:Not established/determined
• Log K_{benzene-water}:
  Not established/determined
• Log K_ow (estimated):
  4. 05
• Melting Point:
  383°F (195°C)
• Molecular Mass:
  277.59

• Soluble In: Slightly soluble in benzene, xylene, carbon tetrachloride
• Specific Gravity:
  Not established/determined
• Vapor Pressure:
  2 x 10^-13 mm Hg at 68°F (20°C)
• Volatility:
  19,300 mg/m³ at 32°F (0°C)
  26,000 to 120,000 mg/m³ at 68°F (20°C)
  72,500 to 143,000 mg/m³ at 77°F (25°C)

Hazardous Materials Warning Labels/Placards

• Shipping Name:
  Diphenylamine chloroarsine
• Identification Number:
  1698 (Guide 154)
• Hazardous Class or Division:
  6.1
• Subsidiary Hazardous Class or Division:
• Label:
  Poison (Toxic)
• Placard Image:

Trade Names and Other Synonyms

• Adamsit
• Chloro diphenylaminearsine
• Diphenylamine chloroarsine
• Diphenylaminechloroarsine

• Fenarsazinchlorid [Czech]
• Phenarsazine chloride
• Phenarsazine, 10-chloro-5,10-dihydro-
• Phenazarsine chloride

In the event of a poison emergency, call the poison center immediately at 1-800-222-1222. If the person who is poisoned cannot wake up, has a hard time breathing, or has convulsions, call 911 emergency services.

For information on who to contact in an emergency, see the CDC website at emergency.cdc.gov or call the CDC public response hotline at (888) 246-2675 (English), (888) 246-2857 (Español), or (866) 874-2646 (TTY).

The user should verify compliance of the cards with the relevant STATE or TERRITORY legislation before use. NIOSH, CDC 2003.

Attention carbon monoxide!

Carbon monoxide poisoning is one of the most common causes of deaths from domestic use of natural gas.

What do you need to know about the combustion process in order not to burn yourself?

Carbon monoxide, poisonous to humans, is produced by the incomplete combustion of any fuel.

Combustion is a chemical reaction in which hydrocarbons present in the fuel react with oxygen contained in the air. With the complete combustion of fuel, whether it is wood, coal, fuel oil or natural gas, almost harmless carbon dioxide (CO2) and water vapor enter the environment along with the heat and smoke generated.

When natural gas is completely burned, the burner flame is visually light blue or bluish-violet.

If, due to an insufficient amount of air, the combustion of the fuel does not occur completely, then combustible substances are released – hydrogen, soot, as well as carbon monoxide, which is deadly for humans – it is also carbon monoxide (CO).

In case of incomplete combustion, soot tongues can be seen in the flame.

Silent killer

Carbon monoxide is often referred to as the “silent killer”. It has no color, no taste, no smell. At the same time, it spreads very quickly, mixing with air without losing its toxic properties. Entering the body during breathing, carbon monoxide penetrates from the lungs into the circulatory system, where it combines with hemoglobin. As a result, the blood loses its ability to carry and deliver oxygen to the tissues, and the body very quickly begins to experience a lack of it.

The toxicity of carbon monoxide is very high and is determined by its concentration in the air. The content of CO in the air 0.01-0.02% can cause mild poisoning. The presence of a person for an hour in a room where the concentration of carbon monoxide reaches 0.1% leads to acute poisoning of moderate severity; severe poisoning occurs at a carbon monoxide concentration of 0.3% within half an hour. Death occurs when a person inhales air with 0.4% carbon monoxide for 30 minutes or 0.5% CO for just one minute.

Attention! In case of intensive combustion of fuel in a room with impaired air exchange (with hermetically closed windows and doors, no draft), a lethal concentration of carbon monoxide is sometimes reached in a matter of minutes!

Emergency care for carbon monoxide poisoning

Symptoms of carbon monoxide poisoning, depending on the degree of damage and the general condition of the body, are: dizziness, headache, nausea, vomiting, tinnitus, shortness of breath, cough, watery eyes.

Emergency care at the first signs of poisoning is to immediately stop further penetration of toxic carbon monoxide into the body of the victim. It should be urgently removed from the polluted room, provide access to clean air. Call an ambulance by calling 03. Before the doctor arrives, you can bring a cotton swab moistened with ammonia to your nose, rub your chest, put heating pads on your legs, mustard plasters on your chest and back, and give the victim hot tea or coffee to drink. In case of severe poisoning and lesions of moderate severity, urgent hospitalization is necessary.

Saving air

It is guaranteed to avoid carbon monoxide poisoning in a room where gas appliances are used by ensuring sufficient air flow from the street to the gas burner and good draft in the chimney. According to this principle, modern safe gas boilers and water heaters with a closed combustion chamber work: the air for combustion in them is carried out directly from the street through a separate air duct; combustion products are also removed through an individual chimney and do not come into contact with the room air.

Of particular danger from the point of view of the risks of carbon monoxide poisoning are flowing gas water heaters (columns) with an open combustion chamber without removal of combustion products, which were previously installed in large quantities (including in apartment buildings) and are still used in settlements that are not with centralized hot water supply.

In order to ensure safety when using these speakers, they are provided with forced air injection into the room. However, many residents, carrying out repairs in their apartments, in violation of the operating rules, eventually eliminate such fans, and also significantly worsen air circulation by installing sealed plastic windows and doors.

Unauthorized changes in the air exchange system in rooms often lead to carbon monoxide poisoning even when the gas equipment is working properly!

Things to remember to avoid carbon monoxide poisoning:

1. To avoid carbon monoxide poisoning during operation of gas equipment, be sure to open the vents, slightly open windows to ensure air flow into the room.

2. Hermetic closing of windows and doors while using gas appliances contributes to the burning out of oxygen in the room and leads to incomplete combustion of the fuel – the release of poisonous carbon monoxide.

3. Gas instantaneous water heater is used for short-term heating of water. Its operation in a constant mode increases the risk of poisoning by products of incomplete combustion of fuel.

4. Do not use a gas stove or oven to heat rooms – if there is insufficient air circulation, this can also lead to oxygen burnout in the room and, as a result, to the formation of carbon monoxide.

5. Check the draft before using a geyser or heating boiler.

First Aid Instructions

First Aid Procedures

​

STEP 1. Remove victim to fresh air. After that, you should immediately call a team of doctors. Do not forget to shut off the methane supply by turning off the burners. If the victim is unable to move, all windows and doors in the apartment should be opened to allow fresh air to enter.

​

STEP 2. Loosen clothing, open the airway, making sure that the tongue does not sink.

​

STEP 3. Lay the casualty down (legs should be higher than the body). Apply cold to the head.

STEP 4. Rub the body and chest, cover warmly and let the ammonia smell.

STEP 5. If vomiting occurs, turn to side.

STEP 6. When breathing stops or slows (up to 8 breaths per minute), begin rescue breathing. In order not to poison yourself, “inhale” through a wet gauze bandage (handkerchief), and when the victim exhales, deviate to the side.

After making sure that the life of the victim is no longer in danger, you need to give him plenty of drink (water without gas, tea, kefir, milk) and a sorbent.

By following these recommendations, you will protect the victim from the development of severe consequences of methane intoxication, and possibly save his life.

The most common household gas is methane. It is relatively low-toxic and lighter than air, so in open space the gas simply rises and does not enter the lungs. However, it is completely different – enclosed spaces, where it can accumulate for a long time without hindrance. Gas poisoning is extremely dangerous and can be fatal.

​

In order to avoid poisoning caused by natural gas, it is necessary to know the properties of the gas and the symptoms of poisoning.

Methane is odorless and completely transparent. It should be borne in mind that the typical “gas smell” inherent in household gas is usually caused by a special additive – methyl mercaptan gas in a small concentration. However, this odor may not be perceived by people with a poor sense of smell. When methane burns, a bluish glow is observed. In a certain quantitative ratio with air, it becomes explosive.

​

This gas has one unpleasant property – it easily penetrates the blood-brain barrier and directly affects the brain. At the same time, it depresses the respiratory system. There is also damage to the CNS. This entails the development of oxygen starvation. If appropriate measures are not taken in a timely manner, gas poisoning and, as a result, death will occur.

​

Symptoms to look out for first.

In practice, a common symptom indicating that domestic gas poisoning has begun is a headache. It is aching and dull in nature, has no specific localization. Far from always, such pain can be associated with poisoning, but is attributed to other reasons – overwork, a cold.

​

Another symptom that people often ignore is chest pain. It can also be attributed to other diseases – ischemia, osteochondrosis, VVD.

​

A common symptom of gas poisoning is dizziness, disorientation and loss of control. This may be expressed in the inability to hold objects in the hands, a staggering gait. In addition, a large concentration of gas in the air usually provokes bouts of nausea and uncontrolled vomiting.

​

Remember that household gas poisoning develops very quickly, and the time from the onset of intoxication to loss of consciousness can take a few minutes. In this case, you should immediately leave the room for fresh air and consult a doctor.