Structural and vascular permeability abnormalities associated with lacunes of the human brain

Histopathological and immune-histochemical studies were carried out in four cases with multiple lacunes of the central grey matter and in control cases without such lesions. Routine light microscopic techniques were applied on paraffin-embedded material to identify lesions that may represent developing lacunes. In addition, polyclonal antisera to human albumin, IgG, fibrinogen and fibronectin were chosen as markers for extravasated plasma proteins. The brain tissue between lacunes contained several forms of focal injuries which may represent precursors of lacunes. Such lesions included foci of status spongiosus and status cribrosus, regions with dilated extracellular spaces and astrocytic gliosis, and multi-locular cysts. These "lacune-associated lesions" often included albumin immune-reactivity in extracellular spaces, nerve cell bodies and astrocytes. Less frequently signs of extravasated IgG, fibrinogen and fibronectin were identified. Thus, lacunes of the human brain frequently showed signs of antigenic sites to albumin. The extracellular deposits probably represent extravasated material from the blood. Vasogenic and cytotoxic oedema combined with other factors probably play important roles during the formation of some of the lacunes.     

Massive ovarian oedema

Eighteen cases of massive ovarian oedema are presented. The age of patients averaged 26 years and 16 presented with an acute abdomen. Hormonal symptoms included virilism in three cases and one with precocious pseudopuberty. Ultrasonographic findings were variable and not diagnostically accurate. When performed, CA 125 levels were not raised. Seventy-two percent of cases occurred in the right ovary and none were bilateral. Torsion occurred in 14 cases. Salpingo-oophorectomy was performed in all cases.
To elucidate its pathogenesis, be this either due to intermittent chronic torsion or to a proliferative phenomenon, immunohistochemistry for Ki-67 and PCNA proliferation antigens, alpha-actin and oestrogen and progesterone receptors was performed. The Ki-67 proliferation index ranged between 0% and 3%, demonstrating the low proliferative status of stromal cells. The PCNA indices, however, were unusually high (60% and above). The divergence between these findings is explained by the fact that PCNA positivity may be related to nuclear reparation subsequent to ischaemia. Alpha-actin was consistently positive in stromal cells, reflecting a myofibroblastic transformation of these cells. These findings together with the clinical evidence of torsion in the majority of cases, lead us to consider that ovarian oedema is a reactive, non-proliferative state of specific stromal cells, occurring as a response to torsion and subsequent ischaemia. The stromal cells have positive oestrogen and progesterone receptors and may undergo stimulatory changes responsible for the hormonally related symptoms often found associated with massive ovarian oedema.     

Hydrogen Sulphide

Hydrogen sulphide (H₂S is the primary chemical hazard in naturalgas production in ‘sour’ gas fields. It is alsoa hazard in sewage treatment and manure-containment operations,construction in wetlands, pelt processing, certain types ofpulp and paper production, and any situation in which organicmaterial decays or inorganic sulphides exist under reducingconditions. H₂S dissociates into free sulphide in the circulation.Sulphide binds to many macromolecules, among them cytochromeoxidase. Although this is undoubtedly an important mechanismof toxicity due to H₂S, there may be others. H₂S provides littleopportunity for escape at high concentrations because of theolfactory paralysis it causes, the steep exposure-response relationships,and the characteristically sudden loss of consciousness it cancause which is colloquially termed ‘knockdown.’Other effects may include mucosal irritation, which is associatedat lower concentrations with a keratoconjunctivitis called ‘gaseye’ and at higher concentrations with risk of pulmonaryoedema. Chronic central nervous system sequelae may possiblyfollow repeated knockdowns: this is controversial and the primaryeffects of H₂S may be confounded by anoxia or head trauma. Treatmentis currently empirical, with a combination of nitrite and hyperbaricoxygen preferred. The treatment regimen is not ideal and carriessome risk.     

Massive ovarian oedema with production of testosterone

Summary Clinical, biochemical, light- and electron microscopic, and immunocytochemical findings of a 13 1/2 year old girl with delayed menarche and signs of virilization due to massive oedema of the left ovary with activation of stromal cells (hyperthecosis) are presented. Testosterone and oestradiol production by large cells in the voluminous ovary was demonstrated by immunocytochemistry and radioimmunoassay. Massive ovarian oedema may result from partial or intermittent torsion of the mesovary interfering with venous and lymphatic drainage, but not with arterial blood flow.     

Pronounced and rapid plasma volume reduction upon quiet standing as revealed by a novel approach to the determination of the intravascular volume change

Plasma volume (PV) changes to 15 min quiet standing were analysed (Hb/Hct-alterations) in two studies (nine and 11 healthy males). Data confirmed and extended our findings that blood, arterial or venous, sampled on standing fails to reveal the induced overall haemoconcentration (PV loss). First, standing led to markedly incomplete mixing of blood between circulatory compartments. Secondly, with sampling of antecubital venous blood, haemoconcentration was strongly affected by regional plasma loss and, apparently equally important, by regional blood flow. These difficulties were circumvented, however, by the finding that the PV restitution (haemoconcentration) in the recumbent subject after standing fitted invariably a monoexponential function with striking precision. It allowed, by extrapolation, a seemingly superior definition of the PV reduction at the very end of standing as supported by the fact that PV changes from Hb/Hct and from IgM protein concentration changes were similar, refuting that F_cell-changes contributed to the pronounced Hb/Hct changes. The described novel approach revealed a nicely reproducible PV loss of no less than 692 ± 46 mL (18.1 ±0.6%, Study I; 18.4 ± 0.5%, Study II), or ± 11% reduction of blood volume, showing that quiet standing leads to a much more rapid and haemodynamically important decrease in PV than reported previously. Yet, PV was virtually restored within 20 min of recumbency after standing, with 50% recovery within 6 min and regain of as much as 70 mL in the very first min. The latter data indicate that the body possesses a surprising capacity for rapid fluid transfer from the extra- to the intravascular space.     

Hereditary angioneurotic oedema

Hereditary angioedema (HAE) is characterised by episodic swelling of the extremities, face, larynx and recurrent abdominal pain, which can mimic the acute abdomen. Trauma of the larynx may result in acute airway obstruction. The management of emergency anaesthesia for Caesarean section of a patient with documented HAE is described and the special problems presented discussed. The methods of prophylaxis available are considered and the use of fresh frozen plasma advocated.     

Acute pulmonary oedema due to transient myocardial dysfunction: an uncommon cause of respiratory distress in the term neonate

Acute postnatal pulmonary oedema due to transient myocardial dysfunction is an uncommon cause of respiratory distress in neonates. Among 11,732 liveborns we observed 3 term neonates with this condition requiring mechanical ventilation. After a delivery mildly to moderately suggestive of subpartum hypoxia, good adaptation and a short symptom free interval all three infants presented with tachydyspnoea, cyanosis, haemorrhagic pulmonary secretions at intubation and pleural effusions, pulmonary venous congestion and patchy alveolar opacities in the first chest radiograph. No evidence of hypoxic-ischaemic encephalopathy was present. The initial need for high ventilatory support and high FiO₂ was followed by rapid recovery after only a couple of hours. In two cases an underlying transient myocardial dysfunction could be demonstrated by echocardiography. Conclusion Pulmonary oedema due to transient myocardial dysfunction can be a rare cause in the differential diagnosis of respiratory distress of the newborn. Myocardial impairment after probable hypoxia can be present without concomitant encephalopathy. Received: 9 January 1997 and in revised form: 18 May 1997 / Accepted: 21 May 1997     

Laryngeal oedema from a neck haematoma A complication of internal jugular vein cannulation

Laryngeal oedema occurred after formation of a neck haematoma after attempted internal jugular vein cannulation. This resulted in complete respiratory obstruction and respiratory arrest and it was impossible to ventilate her lungs manually or intubate her trachea. Oxygenation of the patient was only possible using transtracheal ventilation.     

Non-invasive methods for determination of oedema and water behaviour in the skin

Background/Aim: In an accompanying review, Mani and coworkers discuss methods for measurement of global oedema of the limb. Here, we have concentrated on methodology enabling investigation of oedema and water compartment selectively in the skin and its layers. Results of the studies with magnetic resonance and ultrasound based methods are reviewed.
Conclusion: The behaviour of water in normal young and aged skin has been characterised with magnetic resonance and ultrasonography. Little is yet known about water distribution and behaviour in skin oedema characteristic e.g. for the post-thrombotic syndrome and lymphoedema. Further research in this field is likely to be carried out in the future.     

Cerebral oedema and the fat embolism syndrome

A 19-year-old woman who sustained multiple trauma, but no head injury, developed, the fat embolism syndrome. Her severe, fulminant and reversible neurological deterioration was associated with cerebral oedema. We suggest that cerebral oedema may contribute to the neurological deterioration in the fat embolism syndrome.