Biomedical subjects
Publications and source records attributed to Z Jagodziński.
The authors showed the case of nasal liquorrhoea as post operation complication of nasal septum. The patient had plastic operation of perforation in dura mater.
Authors present 38 patients treated non-operatively because of intracerebral haematomas since 1988 till 1990 in ++Neuro-traumatological Ward Medical Academy of Lódź. The aforementioned data revealed that patients could be treated non-invasively if: 1. On admittance to the ward they were in good general condition they were conscious or their awareness was uptuned a bit. 2. Compression of ventricular system and even slight replacement of media line structures was not an indication to operative treatment if the consciousness of the patients had been good, had not deteriorated during the treatment and on CT scan control haematomas and mass effect vanished. 3. It seemed that if general and neurological condition of patients was good or improved the control could be performed in week or even longer periods of time.
The authors compared the results of a retrospective analysis of two groups of head-injured patients who had coexistent pelvic or lower extremity fractures. One group was treated with early osteosynthesis within the first 12 hours after trauma, simultaneously with neurosurgical treatment, while the second group was treated neurosurgically and osteosynthesis was postponed for 4 to 10 days. The second group revealed a higher mortality, which was due to fat embolism. We conclude that early osteosynthesis is the treatment of choice in patients with coexistent head injury and lower extremity fractures.
In previous years many authors stressed the very rare occurrence and difficulties in establishing of early diagnosis in cases of posttraumatic haematomas in the posterior cranial caeity, among them also the intracerebellar ones. The detection rate of this condition has increased greatly after introduction of computed tomography in the diagnosis of complications following craniocerebral trauma, changing also the view on the method of its treatment. Although before the introduction of CT the prevailin view was that all intracerebellar haematomas should be treated sugically the present opinion is that some of them meeting certain criteria (small size, peripheral situation in the cerebellar hemispheres laterally to the midline, absence of symptoms of intracranial hypertension, and the possibility of frequent CT control) may be treated successively without surgical intervention with adwantage to the patient. Two cases are presented in which intracerebellar haematomas were treated conserwatively. The authors review the pertinent literature stressing the criteria which should be considered in the qualification of patients for this management.
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The authors present 5 cases of meningiomas producing apoplectic symptoms, which appeared among 196 meningeal tumors operated upon from 1969 to 1983. In 4 cases the illness simulated acute cerebral ischaemia, the fifth patient presented twice subarachnoid haemorrhage. The authors discuss possible mechanisms of apoplectic course of meningiomas.
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The authors present two cases of large meningiomas of the lateral ventricle. In both cases the first diagnosis of the disease was cerebral ischaemia. Tumours did not produce symptome of intracranial hypertension, and the most common symptoms of these tumours - hemianopia and papilloedema - were also not observed. Both tumours did not originate from the choroid plexus, probably developing from the tela conjunctiva of the vessels.
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The authors present the results of investigations of the effects of acceleration craniocerebral injury in rats on PaO2 and resulting central nervous system hypoxia. PaO2 fall by 30% of the control value occurred in 25% of rats and in the group of most severe injury this fall amounted to 36% already 1 minute after injury. After 4 minutes this fall rose to 70%. In all animals with injury-induced hypoxia autopsy examination demonstrated on gross inspection acute pulmonary oedema: the weight of the lungs and the lung-body weight index were nearly twice as high as in the animals without oedema. The authors discuss the possible pathological mechanisms of acute neurogenic lung oedema and reach the conclusion that it may be due to excessive, pathological discharge of the sympathetic nervous system. Since the intracranial part of the vascular bed in rats reacts to acceleration trauma with acute spasm, it may be that this factor, together with central nervous system hypoxia caused by neurogenic lung oedema may play a significant role in traumatic secondary central nervous system injury. This risk occurs also in humans with severe brain stem trauma.
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