Respiratory system failure

If symptoms do not improve, the patient should be evaluated for persistent infection. There are many reasons for poor patient outcome with intraabdominal infection improper antimicrobial selection is only one. The patient maybe immunocompromised, which decreases the likelihood of successful outcome with any regimen. It is impossible for antimicrobials to compensate for a nonfunctioning immune system. There may be surgical reasons for poor patient outcome. Failure to identify all intraabdominal foci of infection or leaks from a GI anastomosis may cause continued intraabdominal infection. Even when intraabdominal infection is controlled, accompanying organ system failure, most often renal or respiratory, may lead to patient demise. 

Symptoms of intoxication in humans caused by accidental ingestion of Kou-Wen plants have been described as follows. The effect on the digestive system starts with loss of appetite and turn of the stomach, and continues to severe abdominal pain and intestinal bleeding. The effect on the respiratory system presents as breathing difficulties which finally lead to death by respiratory failure. The effect on muscle innervation usually results in generalized muscular weakness and paralysis of the limbs. The effect on the circulatory system starts with heartbeat disorders and a drop in blood pressure, but heart failure is not a common cause of death. In addition to dilation of pupils, a drop in body temperature and proliferation of white blood cells have also been obseryed (70). 

Highly toxic. Causes skin, eye, and respiratory system mutation. Acute effects include anorexia, nausea, vomiting, diarrhea, excessive salivation, pupillary constriction, broncho constriction, muscle twitching, convulsions, coma, respiratory failure. Special precautions are necessary to prevent inhalation and skin contamination.1 LD50 (oral rat) 13 mg/kg. LD50 (dermal rat) 21 mg/kg. LC50 (rainbow trout, 96 hours) 1.5 mg/L.3 TLV-TWA 0.1 mg/m3.4... 

In indications such as diseases of the central nervous system (CNS), the respiratory system, or the cardiovascular system, failure is often through the emergence of side effects. This is because the intended targets have other biological functions in other organ systems. The side effects come directly Irom the biology of the systems, they are mechanism-based. ... 

The disease appeared after a latent period of at least one to two weeks, longer in some cases, and an apparent relationship between the extent of use of the oil and the effect (a dose-response relationship) was noted in one report. The syndrome had an initial phase lasting one to two months, with effects mainly on the respiratory system and the accumulation of fluid in the lungs. There were many deaths at this early stage from respiratory failure. In the next phase (two to four months) there was muscle pain and liver damage. In the final phase there was muscle wasting and weight loss and the skin was affected (see box). 

High blood levels after topical application or injection of anesthetics may potentially cause systemic reactions. Toxic effects may appear in the central nervous system (CNS), cardiovascular system, or respiratory system. CNS toxicity appears initially as stimulation and may manifest itself clinically as nervousness, tremors, or convulsions. CNS depression, observed clinically as loss of consciousness and depression of respiration, usually follows. The earliest signs of cardiovascular involvement are hypertension, tachycardia, and, occasionally, cardiac arrhythmias. Late cardiovascular signs are hypotension, absent pulse, and weak or absent heartbeat. The effects on the cardiovascular system can develop either simultaneously with CNS depression or alone. If allowed to continue, such cardiac depression and resultant peripheral vasodilation are followed by secondary respiratory failure. 

Chapter 24. Cardiac arrhythmia and cardiac failure Chapter 25. Hyperlipidaemias Chapter 26. Kidney and urinary tract Chapter 27. Respiratory system... 

Excretion is the process by which drugs are eliminated from the body. Excretion occurs primarily via the kidneys, although other routes include the gastrointestinal tract, the respiratory system, and sweat, saliva, and breast milk. Adequate excretion is dependent on effective kidney function. Disease- or drug-induced damage to the kidneys can lead to kidney failure, resulting in a toxic accumulation of medications in the bloodstream. 

Exposure to carbonyl sulfide in animals produces serious nervous system effects with narcotic effects and acute respiratory failure at high concentrations. Acute inhalation exposure to carbonyl sulfide produced nervous system dysfunction and lower respiratory system irritation in rats. Rats exposed to carbonyl sulfide via inhalation for 4 h showed some central nervous system effects at 1062 and 1189 ppm. Results showed hypoactivity, lacrimation, breathing difficulties, cyanosis, bleeding from the nose, convulsions, tremors, and behavioral abnormalities, the most prominent of which, circling. 

Chloramines are toxic to the respiratory system, with asthma and chronic bronchitis resulting from repeated exposures. 11,12 In an exposure event I investigated, a woman poured a mixture of ammonia and bleach into a toilet bowl. She experienced respiratory failure and eventually died when she inhaled the resultant fumes. 

Phosgene victims were described as being either blue or grey in colour. Grey victims were the most serious, as the colour represented failure of the respiratory system, rather than the heart, giving these victims the least chance of recovery. The pulse would be very rapid, breathing shallow, and blood pressure very low death usually occurred within 24 hours. For those that managed to recover from such severe exposure, bronchitis and bronchopneumonia were common problems. 

Onset is rapid and the eyes and respiratory system are most affected. Low-level exposure causes tightness of the chest, rhinorrhea and salivation. Dimming of vision due to miosis, eye pain and headache then follow. On examination, the pupils are constricted and the conjunctivae hyperaemic. These effects may last several hours after cessation of exposure and the headache and visual problems several days. In severe cases, salivation and rhinorrhea are more marked, and wheezing and dyspnea are prominent. Other effects, such as abdominal pain, vomiting, involuntary defecation and micturition, weakness, fasciculation and convulsion, follow depending on the degree of systemic absorption. Death may occur from respiratory failure. 

Many, perhaps most, chemical agents exert their lethal effects because of effects on the respiratory system and thus the provision of breathing support is essential. This is because toxic agents produce effects that cause blockage of the air passages, depression and failure of the respiratory control centres in the brain or paralysis of the muscles of respiration. To overcome these combined effects, the emergency medical response must include the ability to be able to clear and support the airway and also to be able to ventilate the lungs artificially when there is respiratory deficiency or arrest. This support is now part of a standard response for advanced life support in both conventional and toxic trauma and is termed TOXALS (Baker, 1996 Department of Health, 2003) (see Box 3). 

Regardless of their subclassification, all of these compounds have the identical mechanism of action, which is inhibition of acetylcholinesterase at nerve junctions where the molecule acetylcholine is the neuotransmitter. Most acute signs of toxicity are expressed as uncontrollable activity of the nervous system, which clinically is presented as salivation, lacrimation, urination, defecation, and dyspnea. After lethal doses, death results from failure of the respiratory system. Variations in the specific nerves affected, in how the body metabolizes the individual chemical, in where the chemical enters the body, and in the route of administration employed will change the specific clinical presentation seen for an individual exposure scenario. 

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