Pulmonary insufficiency

Bacterial products such as lipopolysaccharides (endotoxins) and cytokines (IL-2) are able to activate the contact system in vitro and in vivo (D9, H4, H7, M41). Immediately after severe trauma or after surgical intervention and particularly during sepsis, a reduction of plasma contact system proteins has been found (C10, K1, N9). Gel filtration studies of plasma demonstrated that plasma PK after activation becomes complexed with a2-M and Cl-Inh (W4). These complexes are rapidly eliminated from the circulation in vivo. In experimental studies in which pulmonary insufficiency was induced in dogs, a significant reduction of plasma kallikrein inhibitors was observed together with reduced HMK. Analysis of the relation be-... 

The combination of hypoxia and hypercapnia in pulmonary insufficiency results in cerebral vasodilation and increased CBF and may lead to increased intracranial pressure. Arteriovenous differences for oxygen across the brain generally decrease as a function of increased CBF, leaving CMR02 unchanged [6]. 

Frequent monitoring for signs of hepatorenal syndrome, pulmonary insufficiency, and endocrine dysfunction is necessary. 

Cor pulmonare Heart disease developed as a result of pulmonary insufficiency latter part of the disease sequence of asbestosis reflecting the impaired transfer of oxygen and carbon dioxide through the blood vessels of the lung. 

Malfunctioning of the respiratory centre (raised intracranial pressure, severe pulmonary insufficiency) causes patients to be intolerant of opioids, and indeed any sedative may precipitate respiratory failure. 

In chronic bronchitis, suppressive chemotherapy, generally needed only during the colder months (in temperate, colder regions), may be considered for patients with symptoms of pulmonary insufficiency, recurrent acute exacerbations or permanently purulent sputum. Amoxicillin or trimethoprim is suitable for treatment. 

Acid-base disorders Initial metabolic alkalosis (resulting from decreased urea synthesis with reduced bicarbonate consumption) may be superimposed by respiratory alkalosis as an outcome of disorders in lung function. During the further course, metabolic acidosis (with renal insufficiency) and respiratory acidosis (with pulmonary insufficiency) can be expected. In advanced or severe stages of the disease, lactate acidosis may develop in some 50% of all comatose patients owing to restricted gluconeogenesis. 

Since adverse effects in humans develop within 2-5 minutes of fixation, with features of pulmonary insufficiency, direct pulmonary damage has been... 

Mafenide is a topical sulfonamide that has been used for the treatment of burns but is now obsolete. Its adverse effects include hyperchloremic metabolic acidosis and (possibly) methemoglobinemia (1). Pulmonary insufficiency has been ascribed to mafenide acetate cream (SEDA-8,160). 

Reducing the opportunity for exposure is the first line of defense. After high-dose exposure watch for signs of pulmonary insufficiency and provide ventilation if needed. Monitor for shock and treat if necessary. For eye contamination, flush eyes immediately with water and then irrigate with saline. For ingestion exposure, rinse mouth and use water for dilution if the patient can swallow. Do not use emetics. 

Death may occur between the fifth and tenth day postexposure because of pulmonary insufficiency complicated by a compromised immune response from mustard-induced bone marrow damage. 

Clomethiazole (6)(see Table 5.7) may produce nasal irritation and sneezing on administration, conjunctival irritation, headache, gastrointestinal disturbances, nausea, vomiting, fever, cough, and tachycardia. It is contraindicated in patients with chronic pulmonary insufficiency, renal failure, or liver disease. 

Mustard-related death occurs in about 3% of the casualties who reach a Medical Treatment Facility of those who die, most die 4 or more days after exposure (Gilchrist, 1928). Of the casualties who died, 84% required at least 4 days of hospitalization. The causes of death are pulmonary insufficiency from airway damage, superimposed infection, and sepsis. Rarely, the amount of mustard will be overwhelming and cause death within 1-2 days in these circumstances, death will be due to neurological factors or massive airway damage (Graef et al., 1948 Heully and... 

FIGURE 13.1 Erythema of the chest of an Iranian casualty as it appeared 5 days after his exposure to mustard. He also had a pulmonary injury with an associated hronchopneumonia due to infection with Haemophilus influenzae. The presence of a nasal oxygen catheter is indicative of the pulmonary insufficiency. (Photograph reprinted from Willems J.L., Ann. Med. Milit. Belg., 3S, 13, 1989. With permission.)... 

Abrams SA. Chronic pulmonary insufficiency in children and its effects on growth and development. J Nutr 2001 131 938S-941S. 

In pre-clinical models, GCS-lOO is able to inhibit the metastatic spread of tumor lines to the lung and is able to shrink large tumors. In pre-clinical toxicology studies, the dose limiting effect of GCS-lOO is pulmonary insufficiency. 

Busing M, Mellert J, Greger B, Flopt U. Acute pulmonary insufficiency due to OKT3 therapy. Transplant Proc 1990 22 1779. 

Leib RMP, Davis WN, Brown T, McQuiggan N. Chronic pulmonary insufficiency secondary to silo-filler s disease. Am J Med. 1958 24 471-478. 

The diffuse nature of the vascular pathological process may lead to a requirement for support of several organ systems. Myocardial lesions detected at autopsy reflect cardiac insufficiency antemortem. Pulmonary insufficiency may develop, and, particularly with yellow fever, hepatorenal syndrome is prominent.16... 

Agents associated with acute-onset pulmonary insufficiency ... 

In the event that a circulating clot enters the heart, it will circulate through the pulmonary artery to the lungs, where it will likely cause an obstruction in the capillary. Over time this may lead to pulmonary insufficiency, difficulty in breathing and chest pain, which are symptoms of pulmonary embolism (PE) (Figure 2). 

Serial acid-base determinations performed during the period of total intravenous alimentation showed a chronic respiratory acidosis in almost all the infants. None of these acid-base changes could be related to the infusate rather, they were attributed to the pulmonary insufficiency of the very immature infant. 

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