Clinical significance of herpes simplex virus in the lower respiratory tract of critically ill patients.
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Biomedical subjects
Publications and source records attributed to P G Jorens.
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Intrathecal administration of ionic contrast media may cause severe and fatal neurotoxic reactions due to their hyperosmolarity and ionic nature. They are therefore strictly contraindicated for all radiologic applications involving the central nervous system (e.g., myelography). We present a case in which ioxitalamate was accidentally injected intrathecally. The patient recovered completely due to a combination of the different therapeutic options reported in the literature, including early mechanical ventilation and neuromuscular paralysis, aggressive control of seizures, elevation of head and trunk to prevent cephalad migration of contrast, steroids, cerebrospinal fluid drainage and lavage and prophylactic antibiotics.
BACKGROUND: Cerebral fat embolism syndrome is a rare, but potentially lethal, complication of long bone fractures. Neurological symptoms are variable, and the clinical diagnosis is difficult. The purpose of this case study is to demonstrate the value of diffusion-weighted MRI of the brain for early diagnosis of fat embolism syndrome. Case Description- A non-head-injured 18-year-old woman suffered acute mental status changes 21 hours after an uncomplicated fracture of the left tibia. MRI of the brain was performed 48 hours after injury. T2-weighted images showed multiple nonconfluent areas of high signal intensity, which, on the diffusion-weighted scans, were revealed as bright spots on a dark background ("starfield" pattern). We suggest that this indicates areas of restricted diffusion that are due to cytotoxic edema, resulting from multiple microemboli. CONCLUSIONS: High-intensity lesions in the brain on diffusion-weighted images may serve as an early-appearing and more sensitive indicator of the diagnosis of fat embolism in the clinical context of long bone injury without head trauma.
OBJECTIVE: Neutrophils play a key role in the physiopathogenesis of acute lung injury in general and acute respiratory distress syndrome (ARDS) in particular. To identify the anti-inflammatory mediators with a protective effect on lung tissue damage in ARDS, we correlated the concentration of the Clara cell 16-kD protein (CC16; an inhibitor of neutrophil chemotaxis), angiogenin (an inhibitor of degranulation), and the total radical oxygen neutralizing activity with the amount of elastase (a marker of neutrophil activation) and with the Pao2/Fio2 ratio, which is inversely related to lung injury. SETTING: University hospital. PATIENTS: Patients with ARDS (n = 12) and patients at risk for developing ARDS (n = 14). INTERVENTIONS: Patients underwent bronchoalveolar lavage 12 hrs after diagnosis of ARDS or at-risk status. MEASUREMENTS AND MAIN RESULTS: The amount of CC16 and radical oxygen neutralizing activity was not significantly different in patients with or at risk for ARDS. In contrast, the amount (mean +/- sem) of angiogenin in the bronchoalveolar lavage of ARDS patients (45 +/- 14 ng/mL, n = 12) was increased 11-fold (p <.05) compared with patients at risk for ARDS (4 +/- 1 ng/mL, n = 14). In patients with ARDS, the amount of protein and angiogenin in bronchoalveolar lavage increased with decreasing concentration of CC16 (p <.05). In addition, CC16 correlated with the Pao2/Fio2 ratio (p <.05) and inversely with the amount of elastase (p <.05) and thus may be regarded as a reliable protective agent for lung injury. CONCLUSION: A high concentration of CC16, a natural inhibitor of neutrophil function, decreases neutrophil-mediated lung damage of patients with ARDS. Strategies to increase natural anti-inflammatory agents, and thus influence the disruption of the balance between natural inflammatory and anti-inflammatory or protective factors, could be useful to modulate the tissue destruction and the course of ARDS.
A patient with a history of schizophrenia was admitted to our hospital in an already severe stage of necrotizing fasciitis of the neck, complicated with mediastinitis and gangrene. Later on, he also developed a vena cava superior syndrome and sepsis. In the few cases and small series described in the literature, necrotizing fasciitis of the neck is usually associated with surgery or trauma. Less frequently, an orodental or pharyngeal infection, often innocuous, is the underlying cause. None of these causes could be identified in our patient. Initially, on computer-assisted tomography (CT) scan, a tracheal rupture was suspected, but this diagnosis could not be confirmed on bronchoscopic examination. On gastroscopy, a stenotic oesophageal segment was discovered. Biopsy of this segment showed a poorly differentiated squamous cell carcinoma. The patient died in sepsis. Autopsy confirmed the presence of a large proximal oesophageal tumour with perforation. As far as we know, no case of a necrotizing fasciitis of the neck caused by perforation of a formerly unknown oesophageal carcinoma has been reported. Even mediastinitis, with or without gangrene, is rarely associated with oesophageal cancer, and in the few cases reported it is always due to fistulization after surgery.
We found that 12.1% of Belgian export meat samples from chicken or pork, unrelated to the PCB/dioxin crisis from 1999, contained more than 50 ng polychlorinated biphenyls (PCBs)/g fat and that 6.5% of samples contain more than 20 ng/g fat for the sum of 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and its metabolites. Part of this background contamination stems from imported animal feed ingredients (fish flour and grains), sometimes contaminated by recent use of DDT, as can be deduced from the ratio between DDT and its main metabolite, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE). However, after comparing PCB concentrations in fish flour and grains with those found in meat, we suggest that the high concentrations stem from recycled fat. This is the first paper describing background concentrations of PCBs in animal meat from Belgium.
OBJECTIVE: After implicating Streptococcus pyogenes as causing acute disseminated encephalomyelitis (ADEM) in a child, we wanted to prove that in vivo activation of autoreactive T lymphocytes by superantigens of this Streptococcus contributed to the dramatic demyelination. BACKGROUND: ADEM is a demyelinating disorder of the CNS sharing many similarities with MS. Demyelination in MS is considered to be the result of an autoimmune process mediated by autoreactive T lymphocytes with specificity for myelin antigens. METHODS: Phenotypic analysis and proliferation assays on blood monocytes, as well as isolation of myelin basic protein (MBP)-reactive T-cell lines/clones; and TCR repertorium analysis by PCR-ELISA and cytokine production. RESULTS: 1) The blood T-cell receptor (TCR) repertoire was compatible with in vivo expansion induced by S. pyogenes exotoxins. 2) TCR expression analysis indicated clonal expansion of CD8+ MBP-reactive T cells, suggesting in vivo activation. MBP-reactive T cells showed crossreactivity to S. pyogenes supernatant and exotoxins. 3) Cytokine mRNA quantification of the mononuclear cells revealed a Th2-biased profile. CONCLUSION: In vivo exposure to S. pyogenes may have induced activation of pathogenic myelin reactive T cells, contributing to the dramatic inflammatory demyelination.
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Kawasaki disease (KD) is an uncommon cause of sudden death in young adults in Europe. Angiographically, the disease is characterized by coronary artery aneurysms which can be fully obstructed by acute thrombosis or by progression of the disease. If diagnosis of KD is made, immediate investigation should be made to determine whether ischemia is occurring and if so, to establish optimal time for revascularisation or cardiac transplantation. We describe an 18-year-old Caucasian male who was not previously known to have KD and who suffered from an acute myocardial infarction complicated by ventricular fibrillation, caused by acute thrombosis of a coronary artery aneurysm.
The only way to rescue ischaemic tissue is to re-instate the oxygen supply to the tissue. However reperfusion of the ischaemic area not only oxygenates the tissue but also initiates a cascade of processes, which may in some cases result in temporary dysfunction of the myocardium. In order to devise protective measures, it is essential to understand the mechanisms and the triggers of this reperfusion phenomenon. In this review we will mainly focus on the inflammatory response caused by reperfusion. We will cover the different steps of polymorphonuclear leukocyte activation and will briefly discuss the molecular biology of the receptors involved. The currently used pharmacological medications in acute cardiology will be reviewed and in particular their actions on polymorphonuclear leukocyte activation, adhesion and degranulation. This review is a compilation of the current knowledge in the field and the therapeutic progress in the prevention of reperfusion injury made today.
Oxidative stress in acute respiratory distress syndrome (ARDS) is considered as an important pathophysiological mechanism in acute impairment of lung function. The present study investigated whether a pulmonary oxidant-antioxidant imbalance is indicated by substantial oxidative modification of proteins in bronchoalveolar lavage (BAL) fluid. Oxidatively modified proteins in BAL fluid, as measured by the reduction of protein carbonyl groups with tritiated borohydride, were studied in control subjects, patients with clinically established ARDS, and patients considered at-risk for ARDS because they had had coronary bypass surgery. Subsets of these at-risk patients were pretreated either with methylprednisolone or N-acetylcysteine. The carbonyl content of BAL fluid proteins was greatly increased in ARDS patients (5.0+/-13 nmol carbonyl x mL(-1) BAL fluid; mean+/-SEM; p=0.0004; n=10) and moderately increased in the untreated patients at-risk for ARDS (1.3+/-0.2 nmol x mL(-1); p=0.027; n=19) compared with controls (0.8+/-0.2 nmol x mL(-1); n=12). The two other at-risk groups pretreated either with methylprednisolone or N-acetylcysteine showed carbonyl values that were statistically not different from the controls (1.2+/-0.2 nmol x mL(-1); p=0.13; n=13, and 1.1+/-0.3 nmol x mL(-1); p=0.40; n=8, respectively). These results show that oxidatively modified proteins clearly accumulated in bronchoalveolar lavage fluid of acute respiratory distress syndrome patients, and to a minor extent in untreated at-risk patients. These data suggest a severe oxidant-antioxidant imbalance in acute respiratory distress syndrome.
Dissection of a cerebral blood vessel is a rare complication of acute neurotrauma with a high incidence of morbidity and mortality. We report on a case of a pediatric patient with severe neurological symptoms in whom angiography showed evidence of a basilar artery dissection. The patient was heparinized and recovered uneventfully.
Alveolar macrophages were isolated by pulmonary lavage from rats which had been either chronically overloaded with iron by intraperitoneal injections of iron dextran for four weeks, or rendered alcoholic by administration of increasing concentrations of alcohol vapour, also for four weeks. Although the hepatic iron content increased in both groups of animals, only the macrophages isolated from the iron-loaded animals showed a significant increase in iron content (P = < 0.05). Furthermore, in these macrophages there was a significant increase in oxidative tone as demonstrated by a six fold increase in superoxide dismutase activity. In both the iron-loaded and chronically alcoholised macrophages, there was a significant diminution in nitric oxide release after stimulation with lipopolysaccharide and/or interferon-gamma, which impaired the ability of both of these groups of macrophages to inhibit the germination of spores from the fungus Rhizopus, a nitric oxide-dependent process. Such an alteration in nitric oxide release reduces the macrophage's microbicidal activity.
We report on two patients with biliary tract injury and associated biloma following blunt abdominal trauma. Both patients underwent emergency surgery because of hemodynamic instability and bloody peritoneal aspiration. Computed tomography in the postoperative days showed severe hepatic parenchymal injury and the presence of hypodense collections with intraparenchymal and subcapsular extension, suggestive for biloma, but otherwise failed to demonstrate the exact location of the bile duct injury. One of them underwent temporary percutaneous drainage. Bile duct injury was well demonstrated on endoscopic retrograde cholangiography (ERCP) and treated by endobiliary stent placement. This report advocates the use of ERCP and endobiliary stenting in the management of biliary injury resulting from liver trauma.
Immunohistochemistry (IHC) and in situ hybridization (ISH) was used to localize extracellular superoxide dismutase (EC-SOD) and its mRNA in rat lung before and after a lipopolysaccharide (LPS)- and hyperoxia-induced inflammation. In control rats, EC-SOD mRNA was synthesized in macrophages and in cells of the arterial vessel walls and the alveolar septa. The EC-SOD protein was mainly localized in plasma and on the apical side of the epithelial cells located near bronchus-associated lymphoid tissue (BALT). ISH did not reveal major changes in the distribution of EC-SOD mRNA upon induction of inflammation. In contrast, IHC demonstrated a progressive staining of the epithelium of the larger bronchi for the protein. Neutrophils and macrophages invading the lung showed an intensive staining for the EC-SOD protein concomitantly with a decrease of the enzyme in the plasma. Twenty-four hours after LPS stimulation only a spotty positivity remained on neutrophils in and between the alveolar spaces. In the bronchoalveolar lavage fluid (BALF), only macrophages showed a strong positivity for EC-SOD mRNA while the protein was detected in macrophages and neutrophils. Exposure to hyperoxia did not affect the distribution of EC-SOD mRNA and protein. The presented data demonstrated that in lung tissue the EC-SOD enzyme may have a protective function for activated macrophages, neutrophils, and lympoid tissue-associated epithelial cells.
We report a patient in whom presumed vasospasm of an angiographically normal coronary artery led to severe transmural myocardial ischemia. To our knowledge, this is the first case in which an allergic reaction to locally applied chlorhexidine caused such a severe reaction.
Amitraz, 1,5 di-(2,4-dimethylphenyl)-3-methyl-1,3,5-triaza-penta-1,4-diene, a formamidine pesticide, is used worldwide. It causes side-effects in animals that resemble those caused by pure alpha 2-adrenergic agonist drugs such as clonidine. Data on poisonings in humans are scanty. We report on a case of human poisoning with amitraz with typical signs of alpha 2-adrenoreceptor stimulation.
Lung volume reduction surgery (LVRS) is emerging as a promising and unique therapeutic option for rigorously selected patients with severe debilitating emphysema. A 51 yr old man with generalized emphysema developed bilateral pneumothoraces during his first holiday abroad. Due to respiratory insufficiency, intubation and mechanical ventilation were necessary. In total, six chest tubes were inserted but massive air leak persisted and his respiratory condition deteriorated due to bronchopneumonia and sepsis. The patient was transferred to Belgium. As a last resort, bilateral LVRS was performed through a median sternotomy. The most diseased areas of the upper lobes containing the air leak were resected bilaterally and a pleurectomy was associated. Three months after operation, there was a remarkable improvement in spirometric values with an increase in forced expiratory volume in one second of almost 100%. The results were sustained after a follow-up of 18 months. In this dramatic case, lung volume reduction surgery proved to be effective, and was even a life saving procedure.