Patterns of Injury

Jimenez, S. 1991 Analysis of Patterns of Injury and Disease in an Historic Skeletal Sample from Belleville, Ontario. Master s Thesis, Department of Anthropology, McMaster University, Hamilton, Ontario. 

Ruegg, C.E., Gandolfi, A.J., Nagle, R.B. and Brendel, K. (1987b). Differential patterns of injury to the proximal tuhule of renal cortical slices following in vitro exposure to mercuric chloride, potassium dichromate or hypoxic conditions. Toxicol. Appl. Pharmacol. 90 261-273. 

Although ozone and PAN are considered the two primary phytotoxic oxidants in the photochemical complex, the specific response of plants to many simulated atmospheres suggests the existence of other phytotoxic oxidants. The symptoms associated with many of these reactant mixtures are closely related to those caused by ozone and PAN. In some tests, the mixtures used would not have produced either ozone or PAN. In other cases, leaf age or the pattern of injury on sensitive test plants suggested one or more pollutants other than ozone or PAN. Field injury symptoms often resemble those reported for ozone or PAN, but the response pattern is sufficiently different that accurate diagnosis is difficult. Brennan et al. correlated development of oxidant symptoms with aldehyde concentrations in New Jersey and suggested that aldehyde may be a major phytotoxic component of the photochemical-oxidant complex. The symptoms were probably not responses to the aldehyde, but rather to some compound or group of compounds present under the same conditions as the aldehyde. ... 

Several cases of ticlopidine-induced hepatotoxicity have been reported (27). Between 10 days and 12 weeks after the start of treatment, patients develop jaundice, usually without fever, eosinophilia, or pain. Laboratory tests show a cholestatic or mixed cholestatic-hepatocellular pattern of injury. There is usually clinical and biochemical recovery within 1-11 months. Frank ticlopidine-associated liver injury is uncommon, but in one study, 44% of patients had abnormal liver function tests and about one-half of them had to stop taking the drug (22). 

Cell death occurs by necrosis or apoptosis or both. The target cell determines the pattern of injury, with hepatocyte injury leading to hepatocellular disease and bihary cell injury leading to cholestasis. AH cellular injury induces fibrosis as an adaptive or healing response, with the duration of injury and genetic factors determining whether cirrhosis and ultimately carcinoma occur (Figure 47-13). 

Laboratory tests are helpful in distinguishing the (1) pattern of injury (hepatocellular versus cholestatic), (2) chronicity of injury (acute versus chronic), and (3) severity of injury (mild versus severe). In general, the aminotransferase enzymes and ALP are used to distinguish the pattern. 

In acute phase, usually the ECG shows at the same time patterns of injury, ischaemia and even necrosis, and in chronic phase there are frequently Q waves and abnormal T waves. These different ECG patterns are not present exactly in the same leads, because although the areas of infarction, injury and ischaemia often coincide, they are not usually identical and especially the injury pattern (ST-segment deviations) in acute phase is present in more leads than is the necrosis pattern (Q wave or equivalent) in chronic phase. 

Therefore, in clinical practice, the same correlation Q waves of necrosis in ECG leads and necrotic areas is used to locate injured areas (ST changes) or ischaemic ones (T-wave changes), although, very often in the acute phase, the ECG patterns of ischaemia and injury are usually visible in more leads than the ECG pattern of necrosis. However, in the chronic phase, the ECG pattern of injury usually... 

Figure 3.3 Left Recordings in case of experimental occlusion of LAD coronary artery in a dog with open heart. (A) Control. (B) ECG pattern of ischaemia (negative T wave). (C) ECG pattern of injury (ST-segment elevation).

When acute coronary occlusion is carried out in experimental animals with closed thorax, it gives rise, during the initial phase of ischaemia, to a delay in repolarisation (TAP) in the subendocardium, which is the area that first suffers ischaemia (Lengyel et al, 1957). This subendocardial ischaemia is evidenced by a tall and peaked T wave immediately followed by ST-segment elevation (injury pattern) if the occlusion persists and the ischaemia becomes severe and transmural (see ECG pattern of injury p. 55). This pattern maybe self-limited if the occlusion is temporary, as in coronary spasm (Prinzmetal... 

The electrocardiographic pattern of injury is recorded from the myocardial area in which, as a consequence of diminished blood supply (more important than the one that generates the ECG pattern of ischaemia) or other non-ischaemic causes, an evident diastolic cellular depolarisation exists (Figure 2.1(3)). This leads to the formation of a low-quality TAP in the injury area which is expressed in the ECG as ST-segment depression or elevation (see Experimental point of view - below - and Figure 4.5). This ECG pattern usually represents especially in the setting of ACS and especially, when the changes are dynamic, the existence of active ischaemia. 

We will firstly refer to cases with normal QRS complex and later on we will briefly comment on how the presence of an ECG pattern of injury may be suspected in patients with wide QRS. 

CHAPTER 4 Electrocardiographic pattern of injury ST-segment abnormalities 57... 

---