Intracranial hemorrhage: diagnosis and emergency management

Intracranial hemorrhages are an important cause of acute neurologic disease presenting in the emergency setting. To optimize outcome, it is important that the physician quickly recognize intracranial hemorrhages. To minimize mortality and neurologic morbidity, it is often necessary to initiate urgent therapy in the emergency rooms and to obtain neurosurgical consultation in order to pursue early surgical therapy. This article discusses the recognition and early treatment of the various types of intracranial hemorrhages.     

Subarachnoid hemorrhage: etiologic variants, pathogenetic features and morphology

8 etiological variants of subarachnoidal hemorrhage are considered, its complications (rupture into the ventricles, development of the arterial spasm, brain edema) and sequelae (aseptic leptomeningitis, external hydrocephaly). Three stages in the subarachnoidal hemorrhage course are distinguished. The analysis of the vascular alterations and ventricular ependyma in cases of the rupture into the brain ventricles is performed. The study of morphological substrates of the liquor circulation in both macro- and microscopical level is recommended in all cases of subarachnoidal hemorrhage.     

Catheter-related infection: an update on diagnosis, treatment, and prevention

PURPOSE: Neoadjuvant chemotherapy is becoming the standard of care for locally advanced breast cancer. This study was performed to determine whether pathologic primary tumor response to neoadjuvant chemotherapy might predict axillary lymph node status and so be used to identify patients in whom surgery could be effectively limited to biopsy of the previous primary tumor site without axillary dissection. PATIENTS AND METHODS: Between 1992 and 1996, 170 consecutive patients with locally advanced breast cancer were treated in a prospective trial with four preoperative cycles of 5-fluorouracil, doxorubicin, and cyclophosphamide. Disease was staged before initiation of preoperative chemotherapy and before surgery. Segmental resection with axillary lymph node dissection or modified radical mastectomy was performed first, followed by postoperative chemotherapy and radiation therapy of the breast (or chest wall) and regional lymphatics. Patient and tumor characteristics associated with complete versus incomplete pathologic primary tumor response to neoadjuvant chemotherapy and correlation between primary breast tumor pathologic response and axillary lymph node status found at surgery were analyzed. RESULTS: Of 156 evaluable patients, 30 patients (19%) had primary breast tumors that were completely eliminated after induction chemotherapy based on histologic assessment. Nineteen of those 30 patients (63%) had negative axillary lymph nodes at dissection, compared with 13 patients (33%) of the 40 who had a near-complete pathologic primary tumor response (< or = 1 cm3 remaining) and only 15 patients (17%) of the 86 who had > 1 cm3 tumor remaining in the pathology specimen of the breast primary. Of the 22 patients with a complete pathologic response in the breast and a clinically negative axilla after induction chemotherapy, axillary dissection revealed positive lymph nodes in four. These four patients had only one or two positive lymph nodes. DISCUSSION: Because initial clinical regression of primary tumor with neoadjuvant chemotherapy is considered an excellent prognostic indicator and because patients with locally advanced breast cancer routinely receive local and regional radiation treatment followed by additional chemotherapy, the role of breast and axillary surgery has been questioned. In this study, a complete pathologic response of the primary tumor to induction chemotherapy is highly predictive of negative axillary lymph node status. Therefore, axillary lymph node dissection may be omitted in certain subsets of patients who have a biopsy-proven complete pathologic response in the primary tumor and a clinical negative axillary examination. Further prospective, randomized investigation is needed to confirm this finding.     

Subarachnoid hemorrhage: protective hypotension in delayed surgery

Systemic hypertension is frequently observed in patients with subarachnoid haemorrhage (SAH). Continuing systemic hypertension might augment the risk of rebleeding and also increase the blood flow and blood volume, resulting in more marked cerebral edema and intracranial hypertension. However, reduction of blood pressure might also decrease cerebral perfusion pressure in patient with an impaired autoregulation and in this way enhance the risk of cerebral ischemia. Anti-hypertensive therapy is not recommended to prevent rebleeding after SAH. The agents of choice for reduction of arterial blood pressure might be mixed alfa and beta adrenergic antagonists and barbiturates.     

Subarachnoid hemorrhage and pontine hemorrhage followed by an embolization procedure of left occipital giant arteriovenous malformation: a case report

A 42-year-old woman suddenly developed headache and nausea on July 26, 1991, and the computed tomography (CT) scan showed a moderate-sized hematoma in the left occipital lobe. After one month's conservative treatment, she had recovered to a neurologically intact state. Cerebral angiography demonstrated a giant arteriovenous malformation fed by enlarged branches of the left posterior cerebral artery as well as small branches arising from the middle cerebral artery, anterior cerebral artery and the meningeal branches of the middle meningeal artery and the occipital artery. Preoperative embolization was planned on February 24, 1992. During an attempt at catheterization of the basilar artery and the left posterior cerebral artery with a balloon catheter and a Tracker-18 catheter, the patient complained of an intensification of her headache, nausea and vomiting. So the embolization procedure was stopped. The CT scan taken immediately at that time showed a severe subarachnoid hemorrhage (SAH). She became comatose about 40 minutes later. CT scan taken next day revealed also a complication of the pontine hemorrhage. Neurologically, she had gradually recovered and could communicate with some simple words 3 months after SAH. The total removal of the AVM was performed on May 26, 1992. Postoperative course was uneventful. She showed rapid and remarkable improvement in her neurological state suggesting that the blood flow in the surrounding brain area had been corrected. A blood deficit had no doubt been caused when blood had been stolen by the giant AVM.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bronchial asthma: update on the revised guidelines for diagnosis and management

Bronchial asthma is a chronic disease with variable airway narrowing, respiratory distress, hyper-responsiveness and inflammation. The morbidity and mortality are increasing despite availability of newer diagnostic and therapeutic strategies. The National Institutes of Health recently issued revised guidelines for disease management. The keys to improved care include earlier recognition of the illness, reduced exposure to triggers, careful monitoring, greater use of long-term control medications and improved patient education.     

Bronchiolitis obliterans: pathogenesis, prevention, and management

Increasing early success-post lung transplant has been tempered by the long-term development of histologic bronchiolitis obliterans (OB) or of the progressive airway obstruction which is called bronchiolitis obliterans syndrome (BOS). Multiple lines of evidence suggest that OB/BOS is due to an injury directed against the epithelial cells in the airways of the donor lung by the immune system of the recipient. Acute rejection is the strongest risk factor for the subsequent development of this process. Efforts to prevent or minimize acute rejection may reduce the prevalence of OB/BOS. Results of treatment with augmented immunosuppression have been disappointing but the treatment of complicating infections in the allograft can be beneficial. Multicenter studies are needed to assess the efficacy of new immunosuppressive agents in preventing or treating OB/BOS.     

Autonomic paroxysms: their pathogenesis, diagnosis and treatment

In the article the rules about etiology and pathogenesis of vegetative paroxysms are stated based on careful analysis of the publications of researches as Russian, so foreign authors, and also own experimental and clinical supervision. During experimental and clinical researches the modern methods were used, enabling to estimate from positions of the system analysis different parts of pathogenesis of vegetative paroxysms, and also to offer ways of differential diagnostics of the various forms of disease. The application of some new preparations and direction of therapy of vegetative paroxysms are substantiated, and also the various circuits of treatment of the patients with distinguishing forms of given pathology are motivated.     

The hepatic porphyrias: pathogenesis, manifestations, and management

Sexual activities and attitudes of a group of adolescents, who have been followed from early infancy as a part of the New York Longitudinal Study, are reported. Adolescents in the study evince a more matter-of-fact, less fearful attitude than that of previous generations, but do not seem more prone to casual sexual encounters. Sexual conflicts are seen to occur only in relation to overall psychological conflict.     

Subarachnoid hemorrhage in Vestfold county. Occurrence and prognosis

This prospective study comprises all patients treated for spontaneous non-traumatic subarachnoid haemorrhage between May 1991 and December 1995 in the county of Vestfold, Norway. A total of 76 patients was recorded, giving an incidence of 8.1 per 100 000 per year. Mean age at time of bleeding was 52.7 years. In 36 patients the cause of the bleeding was an intracranial aneurysm; most of the aneurysms were localized to the anterior communicating artery and middle cerebral artery. In seven patients the cause was arteriovenous malformation. 23 patients (30%) died because of their subarachnoid haemorrhage; 15 from the primary bleeding and eight because of re-bleeding. The mortality for patients aged over 60 years was 48%, and for patients younger than 60 years 19%. There was a strict correlation between the initial clinical condition (Hunt & Hess scale) and the final outcome (Glasgow Outcome Scale).     

Osteoporosis: pathogenesis, diagnosis, and treatment in older adults

Prevention of osteoporosis is a major health concern. Bone loss occurs throughout life in both women and men due to calcium deficiency, hormonal deficiency, and changes in bone formation. The diagnosis of osteoporosis can now be made prior to fragility fracture, allowing for prevention as well as treatment. Criteria for diagnosis of osteoporosis are reviewed, and a plan for the evaluation of secondary causes of osteoporosis is discussed. Also reviewed are prevention and treatment options such as exercise, calcium supplementation, hormone replacement, and new and investigational drugs.     

Onychomycosis: recognition, diagnosis, and management

A series of hydroxynaphthazarins has been synthesized. Some of them were found in in vivo experiments to be protectors of myocardium under ischemia-reperfusion and to reduce the infarction zone by 50% without any adverse effect. All compounds exhibit a moderate or small toxicity and are active in low doses.     

Subarachnoid hemorrhage induces c-fos, c-jun and hsp70 mRNA expression in rat brain

To detect stress responses of the brain to subarachnoid hemorrhage (SAH), we investigated the expression of immediate early genes (IEGs) and hsp70 mRNA by in situ hybridization. Experimental SAH was produced in 49 rats by endovascular penetration. We also monitored the intracranial pressure (ICP) changes. The genes c-fos and c-jun were induced in the cerebral cortex, hippocampus and dentate gyrus in the penetrated side. mRNA coding for hsp70 was induced in the cerebral cortex, hippocampus, thalamus, hypothalamus and caudoputamen in the penetrated side and extended to the contralateral hemisphere. IEGs in the cerebral cortex were completely blocked by MK-801 pretreatment, but hsp70 mRNA was not. This suggests that the expression of IEGs correlates with spreading depression. The IEGs and hsp70 expression may reflect the severity of SAH impact and relate to the mechanisms of symptomatic vasospasm.     

Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update

Further preliminary observations are reported of an experiment to examine the spread of infectivity and the occurrence of pathological changes in cattle exposed orally to infection with bovine spongiform encephalopathy. Calves were dosed at four months of age and clinically monitored groups were killed sequentially from two to 40 months after inoculation. Tissues were collected for bioassay, for histopathological examinations and for the detection of PrP. Previous reported observations have included the presence of infectivity in the distal ileum of cattle killed after six to 18 months, the earliest onset of clinical signs in an exposed animal after 35 months, and diagnostic histopathological changes in the brain, in association with clinical disease, after 36, 38 and 40 months. In spite of the relative inefficiency of the bioassay of scrapie-like agents across a species barrier the new observations confirm that the onset of clinical signs and pathological changes in the central nervous system (CNS) occur at approximately the same time. The earliest pathological change, the presence of abnormal PrP 32 months after inoculation, coincided with the earliest detected infectivity in the CNS and occurred shortly before there was evidence of typical spongiform changes in the brain 36 months after inoculation. Infectivity has now been demonstrated in the peripheral nervous system, in the cervical and thoracic dorsal root ganglia 32 to 40 months after inoculation and in the trigeminal ganglion 36 and 38 months after inoculation. At the time of writing evidence of infectivity in other tissues is confined to the distal ileum, not only after six to 18 months but also after 38 and 40 months, but these findings may be supplemented by the results of further mouse assays. Nevertheless, they are in general agreement with current knowledge of the pathogenesis of scrapie.