Difference in neurotransmitter metabolism in frontotemporal-lobe contusion and diffuse cerebral contusion.
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Bacterial infections frequently,complicate pulmonary contusion and are the leading cause of death in such patients. This study evaluated the effects of pulmonary contusion alone and contusion associated with other factors on the ability to clear aerosolized bacteria from the lung. Lung bacterial clearance of Staphylococcus aureus and Klebsiella pneumoniae was studied in animals with isolated pulmonary contusion, or contusion associated with blood loss, rapid crystalloid infusion, or steroid administration. An isolated pulmonary contusion produced no impairment of the ability of the contused lung to clear either gram-negative or gram-positive organisms. The addition of acute blood loss and crystalloid infusion resulted in decreased clearance from the contused lung; steroid administration caused a marked depression in lung bacterial clearance from the noninjured lung as well. The canine model described allowed for study of regional differences in bacterial clearance. The data presented support several conclusions; (1) the contused lung is not more susceptible to bacterial infection than the normal lung: (2) acute blood loss renders the contused lung less able to clear bacteria; (3) crystalloid infusion markedly depresses lung bacterial clearance; and (4) steroids have a deleterious antibacterial effect on both contused and noncontused lungs.
We produced a localized right lower lobe (RLL) contusion in 14 anesthetized ventilated dogs, 7 of which were treated with positive end-expiratory pressure (PEEP group). We measured gas exchange, pulmonary mechanics, and regional function before and 5 h after the contusion. Arterial PO2 decreased by 20 Torr and venous admixture doubled in both groups during air breathing. The shunt fraction (Qs/Qt) was minimally increased, despite a large lobar Qs/Qt (0.43) in the contused RLL. These results were explained by reduced ventilation per unit volume (VA/V), and ventilation-to-perfusion ratios of the contused RLL measured with 133Xe technique. We conclude that pulmonary contusion causes a leak of blood and plasma, flooding 25% of the air spaces of the RLL at FRC, reducing the compliance of adjacent air spaces, and resulting in a reduced VA/V and a large RLL Qs/Qt. These results are consistent with the observed reduction in regional volume and perfusion in the contused RLL, and suggest that Qs/Qt was not increased because blood flow was markedly reduced to flooded air spaces. PEEP reduced the hypoxemia, but increased the contusion.
Can a contusion cause coxarthrosis in the absence of both fracture and dislocation? Yes. To demonstrate this the authors report 6 cases that fulfil the following conditions: (1) Simple but violent contusion affecting the greater trochanter or the knee (dashboard accident) or a forced movement, such as in doing the splits; (2) immediate or slightly delayed pain, generally of short duration (a few weeks); (3) absence of coxarthrogenic malformations and absence of pre-existing signs of a pathological hip condition; (4) progressive coxarthrosis on the side of the contusion; (5) chronological relation between the development of the coxarthrosis images and the date of the contusion; (6) subjects less than 35 years of age, in order to eliminate cases with latent primary pre-coxarthrosis. The average age of the six patients at the start of the coxarthrosis was 24.7 years (range: 13 to 33 years); there were four men and two women. In five of the six cases a violent contusion in the trochanter region was involved as a result of a fall on a hard surface or a traffic accident. In one case a forced movement on landing from a jump was involved. Evolution in three periods is usual: the hip is painful either immediately or after a few weeks (particularly on rising after a period in bed for multiple injuries). This post-traumatic pain lasts from ten days to one month, rarely longer. It is followed by a period free of pain that may last from five months to ten years (average: five years). Subsequently there is pain every day and the onset of the limp associated with coxarthrosis. Radiographically the reduction of the joint space and/or the osteophytosis appears after three months to two years (average: one year). However, there may not be any pain associated with these lesions for a long time. The authors propose that the first five conditions enumerated above represent the essential medico-legal conditions of coxarthrosis by contusion. The restriction as regards age (No 6) was introduced only to show clearly the existence of post-contusive coxarthrosis. However, even if one or more of the medico-legal conditions are not fulfilled the imputability may still be valid. Some such cases are discussed.
A stystematic neurological and electroencephalographical follow-up study in 344 head injured adults gave the following results: 1. 52% of all the hospitalized (mostly primarily amnesic) patients had a cerebral contusion. A contusion was assumed in cases with focal neurological signs (13%), amnesias of more than 8 hours (16%) and/or EEG-abnormalities lasting for more than 24 hours (49%). 2. Traumatic EEG-abnormalities were general slowing (43%) and foci (32%). In 40% of the cases with general slowing the slowing (greater than or equal to 1.5/sec) was within the alpha-frequency band and could only retrospectively be assed. 3. The EEG was invariably abnormal in cases with an amnesia exceeding 8 hours. If the amnesia exceeded 1 hour abnormalities were found in 73%. 4. Among the patients with contusion 6.5% had no amnesia, 48% less than 30 minutes and only 30% an amnesia for more than 8 hours. In 75% of the patients with concussion amnesia lasted less than one hour. 5. Skull fractures were mostly combined with contusion (74%). 6. Impaired drive, reduced ability to concentrate, memory deficits, headache and dizziness were significantly more frequent 6 months after contusion than after concussion. 7. 21% of the patients with traumatic dizziness (44%) had a labyrinthine contusion. 8. Among the contusions diagnosed with the aid of EEG recordings 58% would have been missed after exclusive neurological examination and 82% after application of the classical criteria used by surgeons and general practitioners.
Localized pulmonary contusions were produced in the right lower lobes (RLL) of 12 anesthetized ventilated dogs, 6 of which had a flail segment in the chest wall over the RLL. Pulmonary oxygen exchange during ventilation with air and oxygen, and the lobar distribution of pulmonary perfusion by radioactive microsphere techniques were measured before and 3 h after contusion, and again after thoracotomy. These were compared to 12 noncontused dogs, 6 of which had a flail segment. Contusion produced an average decrease of 20 Torr in Pao2 during air breathing and an average increase in Qs/Qt of less than 5%, surprisingly small given the doubled weight and average 44% shunt calculated in the contused lobe after thoracotomy. No significant effect of flail or thoracotomy was found, indicating that the presence of an intact chest wall and lung-chest wall interdependence was not a major factor preventing a larger increase in intact whole-animal shunt of contused dogs. Rather, the small effect of this severe lobar injury on whole-animal shunt was due to a 30% decrease in RLL relative perfusion. This reduction was demonstrated to be localized to a smaller hemorrhagic subsection of the contused lobe.
At the present writing, the biomechanics of "coup-contrecoup" contusions may be summarized as follows: 1) "Coup" contusions are caused by the slapping effect of discrete areas of inbeding bone during impact. "Contrecoup" contusions are caused by the movements of the brain against irregular and rough bony enviornment. 2) When the head is relatively fixed, a blunt discrete impact causes a "coup" lesion with no "contrecoup" effect. 3) When the head is free to move, a blunt impact will cause a contrecoup lesion or lesions and no "coup" effect. 4) "Fracture contusion" is caused by the slapping effect of the fracture site on the outbending cerebral surface. In such cases, occassionally the dura may be torn. 5) Deeper contusions in the substance of the brain are due to inertial stresses from relative movements and pressure gradients. 6) Contusions of the cerebral tonsils are due to their relative movements at the posterior fossa-foramen magnum junction.
Cardiac contusions are being recognized with frequency. Among 507 patients with non-penetrating chest injuries, 210 had serial electrocardiograms sufficient to evaluate the heart. Forty-five of these 210 patients (21%) had cardiac contusions. These 45 patients and 3 others who were confirmed to have cardiac contusions at necropsy, comprise the 48 patients in this series. Life-indangering cardiac complications occurred in 14 (29%) of the 48 patients, and 4 patients died. The development of cardiac complications following cardiac contusions appears to have a significant relationship to the presence of shock, hypoxia and to factors related to the severity of multiple injuries. These observations have therapeutic implications in management of patients with cardiac contusions through prevention of hypovolemia and hypoxia and avoidance of fluid overload as well as treatment of specific cardiac complications.
Cerebral contusion is considered to be the lesion leading to neurological sequelae of mental retardation and cerebral palsy in abused children. This has been difficult to document other than at autopsy or craniotomy by previously available techniques. Acute contusion or hemorrhage presumably secondary to contusion is readily documented by computed tomography (CT). We are reporting the cases of four children with alleged or suspected abuse and CT evidence of cerebral contusion. The contusion has been found both with and without external evidence of head injury.
A model is described for study of the cerebral edema associated with the contusion of closed head injury. A Remington Humane Stunner was used to deliver blows to the skulls of anesthetized cats. Forty-eight hours after impact, those cats demonstrating a one-sided contusion were tested for cerebral edema by measurement of the decrease in density (specific gravity) of white matter from normal values. Significant change in tissue density was seen in the white matter of contused hemispheres. Hemispheres with contusion limited to the cortex (gray matter) showed a change in tissue density which was considerably less than that seen in hemispheres with contusion involving both gray and white matter.
Myocardial contusion is a serious problem not easily diagnosed. Laboratory and clinical studies carried out on myocardial infarction suggested that Technetium scanning might clarify this diagnostic dilemma. Radionuclide imaging with Technetium was carried out in 29 patients suspected of having myocardial contusion. Of 13 patients in whom contusion was confirmed electrocardiographically, scan was positive in only two. Use of the technique in diagnosis of myocardial contusion is not recommended.
The hemodynamic changes in rabbit eyes following contusion were studied with rheoophthalmography (ROG), in which the wave amplitudes were markedly reduced and then recovered in 3 weeks, while in the anisodine-I treated group they recovered in 2 weeks. Contusion of 3 joules disrupted the choroidal circulation and damaged the retina. Anisodine-I improved the vasomotor functions of the choroidal vessels and was effective in treatment of ocular contusion. ROG was a sensitive objective means of estimating the severity of ocular contusion and evaluating the therapeutic effects.
The uptake of technetium-99m stannous pyrophosphate in contused myocardium was measured as a function of time from the insult. The free wall of the dog's left ventricle was surgically exposed and struck with a spring-loaded paddle. Pyrophosphate was injected intravenously from 1 1/2 to 47 1/2 hr after the injury. After 1/2 hr of incubation the hearts were removed and the Tc-99m content of contused and noncontused myocardium was measured. Pyrophosphate was concentrated in contused myocardium at all of the time periods tested. Contused-to-normal ratios for pyrophosphate uptake ranged from 8.1 (8 hr) to 41.9 (48 hr).
Thirty-four rats were killed by transcardial perfusion fixation 1 min after a contusing concussive head injury, and 17 rats 1 day later. From the results obtained with a new silver method demonstrating traumatically damaged neuronal somata, dendrites and axons the following conclusions were drawn: (1) outside the contused territories all features of traumatically induced neuronal argyrophilia are similar to those found in non-contusing concussive head injury, as reported in an accompanying paper; (2) within contused territories the neuronal argyrophilia is abolished by some substance released either from damaged blood vessels or damage parenchymal cells, while the neuronal damage otherwise underlying the induction of argyrophilia is present; (3) different phenotypes of neurons are vulnerable to different values of the parameters of the intracranial pressure wave generated by the trauma; (4) some of the neurons may recover from the traumatically induced argyrophilic damage; (5) traumatically induced inundation of neurons with extracellular tracers, as reported by other authors, and somato-dendritic argyrophilia may be different manifestations of one and the same phenomenon; and (6) diffuse primary traumatic axonal injury in human neuropathology may be closely correlated to axonal argyrophilia.
Of 20 patients with blunt chest trauma who underwent cardiac scanning, serial electrocardiography and cardiac monitoring to rule out myocardial contusion, four had positive cardiac scans. All four had electrocardiographic abnormalities: three had nonspecific ST-T wave changes, and the fourth had electrocardiographic evidence of an acute subendocardial infarction. Of the 16 patients with negative scans, five had normal electrocardiograms. In the remaining 11 patients, factors other than myocardial contusion were suspected causes of electrocardiographic abnormalities. On the basis of this data, electrocardiogram changes in the traumatized patient have various causes. Cardiac scanning appears to be a useful adjunct to electrocardiography in confirming the presence of myocardial contusion.
A model in the rat for pulmonary contusion after blunt chest trauma is described. It is possible to avoid trauma of the mediastinal organs, liver and spleen; therefore it is possible to produce pulmonary contusion with a good reproducebility. The parameter for the extent of contusion was the lungweight which rose statistically with a specific force of trauma. Simultaneous injection of high doses of prednisolone with the blunt chest trauma inhibits the increase of the lung weight.
Myocardial contusion secondary to nonpenetrating chest trauma can occur in the absence of any identifiable large vessel coronary artery occlusion or injury. It has also been reported in association with coronary artery atheromata, thrombosis, rupture, and fistula formation. After reviewing the clinical and experimental research literature, we conclude that myocardial contusion necrosis results from changes in perfusion of small vessels and the coronary microvasculature. Coronary arteriography and emergency coronary artery bypass surgery do not appear promising as therapeutic modalities to reduce myocardial necrosis in this condition. More appropriate therapeutic emphasis may result from research efforts to develop pharmacologic interventions to preserve contused myocardium similar to those currently being evaluated in the management of patients with ischemic myocardium secondary to coronary artery disease.
The clinical course and prognosis in the event of a severe cerebrocrainial trauma depend, above all, on the extent of the contusion and smashing of the brain sustained. The pathogenetic factor of prime importance determining the severity of the contusion is the development of the local and general cerebral edema. Rapidly accuring edema and turgescence of the brain, rising intracranial pressure lead to the dislocation of the brain attended by a clinical picture of a grave secondary lesion of the brain stem. To eliminate or prevent the emergence of the dislocation syndrome an operative removal of the primary contusion focus and concussory treatment of the brain in combination with the pathogenetic conservative therapy, aimed at preventing further progressive edema of the brain, are indicated in some of such patients.