Necrosis trauma

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

Tetanus occurs when Cl. tetani, ubiquitous in the soil and faeces, contaminates wounds, especially deep puncture-type lesions. These might be minor traumas such as a splinter, or major ones such as battle injury. At these sites, tissue necrosis and possibly microbial growth reduce the oxygen tension to allow this anaerobe to multiply. Its growth is accompanied by the production of a highly potent toxin which passes up peripheral nerves and diSuses locally within the central nervous system. It acts like strychnine by affecting normal function at the synapses. Since the motor nerves of the brain stem are the shortest, the cranial nerves are the first affected, with twitches of the eyes and spasms of the jaw (lockjaw). 

C20. Cinat, M. E., Waxman, K., Granger, G. A., Pearce, W., Annas, C., and Daughters, K., Trauma causes sustained elevation of soluble tumor necrosis factor receptors. J. Am. Coll. Surg. 17, 529-537 (1994). 

Necrosis A pathological process caused by the progressive degradative action of enzymes that is generally associated with severe cellular trauma. It is characterized by mitochondrial swelling, nuclear flocculation, uncontrolled cell lysis, and ultimately cell death. [NIH]... 

An interesting additional point is that during trauma the cytokine, tumour necrosis factor, results in a decrease in lipase activity in adipose and other tissues, so that there is an increase in the level of VLDL and chylomicrons in the blood. The significance of this is unclear but it may be that pathogens in the blood are adsorbed onto the emulsion of VLDL or chylomicrons which reduces the risk of adsorption of the pathogen onto the surface of a cell, which is necessary for the pathogen to enter the ceU. This localisation also aids attack by antibodies (Chapter 17). 

Figure 18.5 A summary of the biochemical, physiological and immunological changes brought about by cytokines in response to trauma. Cytokines can be produced in trauma from macrophages, lymphocytes, endothelial cells in the tissue that is damaged, and also by Kupffer cells if the liver is damaged. IL-1, IL-6 - interleukins 1 and 6 TNF - tumour necrosis factor, IFN - interferon.

Neuronal cell death is required for the development of the nervous system. However, recent studies suggest that neurons die from programmed cell death (apoptosis) in brains deprived of oxygen by stroke [14] and trauma [15], and in the brains of Alzheimer s patients [16], Therefore, prevention of neuronal apoptosis has been considered to be a desirable therapeutic strategy for treating such neurodegenerative diseases, although the value of this approach is not yet evident. We have recently reported that crocin suppresses tumor necrosis factor (TNF)-a-... 

Pancreatic abscess A circumscribed intraabdominal collection of pus, usually in proximity to the pancreas, containing little or no pancreatic necrosis, which arises as a consequence of acute pancreatitis or pancreatic trauma. 

The vast majority of ventricular septal defects (VSD) are congenital. Acquired VSDs are almost always a consequence of septal rupture following myocardial infarction, traumatic VSDs as a consequence of sharp or blunt chest trauma are exceptionally rare. Typically the post myocardial infarction ventricular septal defect (PMIVSD) occurs within the first week after the event (41). In the current era of thrombolysis about 0.2% of patients develop a VSD as a result of septal necrosis. Medical management of these patients is limited and carries a 30-day mortality of 94% compared with 47% who were treated surgically (42). 

C-reactive protein (CRP) is a protein produced by the liver during episodes of acute inflammation. CRP is not a specific test, however, and a positive CRP may indicate a number of things including inflammatory disease, malignancy, muscle necrosis (e.g. myocardial infarction) and trauma, as well as infection. A normal CRP is unlikely in the presence of a bacterial infection and a very high CRP (>100 mg/L) is more likely to occur in bacterial than viral infection. In this case, the patient s high CRP is consistent with a bacterial infection. CRP may be used to monitor a patient s response to therapy. 

Tumour necrosis factor-a (TNFa) accumulates in the brain after trauma. This cytokine is known to be an important factor in delayed CNS damage. It was found that, in addition to its anti-NMDA effect, HU-211 causes up to 90% inhibition of the TNFa surge after closed head injury in rats [195], Bacterial and viral infections of the CNS are known to cause secretion of the TNFa as well as interleukin-1 and other cytokines which are involved in the inflammatory process and may cause secondary damage. Such infections may result in high mortality. It was found that rats infected with Streptococcus pneumoniae suffered less cerebral oedema on treatment with a combination of a suitable antibiotic with HU-211 than the antibiotic alone [196],... 

Intranasal use, a common method of cocaine abuse, can damage the sinonasal tract, causing acute and chronic inflammation, necrosis, and osteocartilaginous erosion (SEDA-17, 36). These conditions occur secondary to the combined effects of direct trauma from instrumentation, vasoconstriction of small blood vessels with resultant ischemic necrosis, and chemical irritation from adulterants. Intranasal cocaine users can develop septal perforation, saddle-nose deformities, and sinonasal structural damage. 

Rogers FB, Li SC. Acute colonic necrosis associated with sodium polystyrene sulfonate (Kayexalate) enemas in a critically ill patient case report and review of the literature. J Trauma 2001 51(2) 395-7. 

In contrast spontaneous cell death or necrosis [302,306] is observed in mammalians after trauma or ischemia cells and their organelles swell, their membranes rupture and then their content effluxes [301]. This process is combined in mammalians with inflammation. 

One important assessment made with NIR is the viability of tissue after trauma [91]. Prolonged and severe tissue hypoxia results in tissue necrosis in pedicled flaps. The group used NIR to identify tissue regions with poor oxygen supply. The work was performed on reversed McFarlane rat dorsal skin flaps. It was seen that oxygen delivery to the flap tissue dropped immediately upon the onset of atopy. As expected, severe trauma that causes severing of the skin from the main blood flow causes necrosis of the tissue. Near-IR may be used as a tool in assessing the success of reattachment of the traumatized skin. 

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