[High-dose magnesium sulfate in the treatment of aconite poisoning]. / Hochdosiertes Magnesiumsulfat bei Aconitumintoxikation.

This article reports the case of a 62-year-old male patient who ingested the roots of Monkshood (Aconitum napellus) and white hellebore (Veratrum album) dissolved in alcohol with a suicidal intention and suffered cardiotoxic and neurotoxic symptoms. After contacting the Poison Information Centre ventricular arrhythmia was treated with high-dose magnesium sulphate as the only antiarrhythmic agent and subsequently a stable sinus rhythm could be established after approximately 3 h. Aconitum napellus is considered the most poisonous plant in Europe and it is found in gardens, the Alps and the Highlands. Poisoning is mainly caused by the alkaloid aconite that leads to persistent opening and activation of voltage-dependent sodium channels resulting in severe cardiac and neurological toxicity. As no specific antidote is known so far, poisoning is associated with a high mortality. The therapy with high-dose magnesium sulphate is based on in vitro and animal experiments as well as limited clinical case reports.

Sclerosing cholangitis and liver cirrhosis after extrabiliary infections: report on three cases.

OBJECTIVE: To describe three unusual cases of sclerosing cholangitis after severe extrahepatic/extrabiliary bacterial infections. DESIGN: Case report, clinical. SETTING: Tertiary care intensive care unit (ICU). PATIENTS: Three patients admitted to the ICU with infections from Gram-positive bacteria followed by sclerosing cholangitis and secondary biliary cirrhosis. MAIN RESULTS: Three unusual cases of persisting cholestasis that occurred after bacterial infections originating from extrahepatic/extrabiliary foci are described. Endoscopic retrograde cholangiopancreatography and magnetic resonance cholangiopancreatography revealed multiple strictures of the intrahepatic bile ducts as a sign of sclerosing cholangitis. All patients progressed to biliary cirrhosis within months after the onset of cholestasis. CONCLUSION: Infection-associated cholestasis is usually a functional disorder and subsides after effective treatment of the underlying inflammatory focus. In rare cases, however, extrahepatic/extrabiliary infections may lead to sclerosing cholangitis and secondary biliary cirrhosis via unknown mechanisms.

Systemic effects and side effects of interstitial techniques used in liver tissue.

BACKGROUND: Percutaneous ethanol injection (PEI) and cryosurgery are increasingly used for the treatment of liver malignancies. To create a safety margin and to destroy completely diffusely growing tumors, the precise destruction of healthy liver tissue is necessary. Little is known about the effects of operating on this type of tissue. This study evaluated the effects and side effects of PEI and cryosurgery when applied to normal parenchyma of the liver. STUDY DESIGN: Two groups of six minipigs each were treated with either PEI or cryosurgery to create necrosis in the liver. During and after the procedures, vital signs were monitored and necrotic areas were observed by ultrasonography. Standard and immunohistochemistry stains were made from samples of the necrosis, the liver, and the lung. RESULTS: In the PEI group, thromboembolic complications occurred in all animals (fatality rate 50%). Hematogenous spread of hepatocytes was demonstrated by immunohistochemistry and was a cause of pulmonary embolism. In the cryosurgery group, neither specific complications nor signs of cell spillage occurred. Because of an isolating effect of blood perfusion, hepatocytes close to the portal triads were less damaged, vital cells were present in the periphery, and the necroses were smaller than the induced lesions. CONCLUSIONS: The effect of PEI in healthy liver tissue is unpredictable. This makes the creation of a safety margin or the treatment of a diffusely infiltrating tumor impossible. PEI always introduces the risk of hematogenous cell spread. Effects of cryosurgery are less dependent on tissue qualities. In both techniques, the real extent of complete tissue destruction cannot be visualized by ultrasonography.

[An unconventional use of the laryngeal mask for the therapy of a postoperative atelectasis-induced respiratory insufficiency]. / Unkonventioneller Einsatz der Kehlkopfmaske zur Therapie einer postoperativen, atelektasenbedingten Ateminsuffizienz.

A 90-year-old cardiopulmonary high-risk patient had to undergo a laparatomy due to a perforated ulcus ventriculi. Postoperatively he developed pulmonary insufficiency due to an atelectasis of the upper right pulmonary region. The clinical situation deteriorated because of dyspnoea and exhaustion. Conservative therapy failed. Atelectasis was overcome by a laryngeal mask airway (LMA) inserted without relaxation and anaesthesia. The LMA enabled CPAP-training for 45 minutes added by inflation of the lung up to a peak airway pressure of 22 cm H2O. Problems and risks of this unconventional use are discussed. Reintubation involving the necessity of relaxation and anaesthesia could be avoided by this unconventional use of a LMA. This case report confirms the good tolerance and easy handling of the LMA. It demonstrates a further application of the LMA, which is not only a new device but a new idea of airway management.

Neurohumoral pathways mediating stress-induced inhibition of gastric acid secretion in rats.

In awake rats, physical restraint inhibited pentagastrin-stimulated gastric acid secretion by more than 50%. This inhibitory effect was abolished by either ganglionic or noradrenergic blockade. Adrenalectomy, as well as pretreatment with a vasopressin V1-receptor antagonist, significantly attenuated the gastric inhibitory effect in response to stress. In contrast, neither truncal vagotomy nor hypophysectomy or opiate blockade prevented stress-induced inhibition of gastric acid secretion. These findings indicate that stress-induced inhibition of gastric acid secretion in rats is mediated by autonomic, noradrenergic efferents as well as by adrenal and vasopressin-dependent pathways. Vagal efferents, opiate pathways, and the pituitary gland do not seem to be involved.

Effects of neuropeptides on gastric acid and duodenal bicarbonate secretions in freely moving rats.

The central nervous system effects of neuropeptides on gastric acid and duodenal bicarbonate secretions were examined. In freely moving rats, i.c.v. administration of thyrotropin-releasing hormone (TRH), human gastrin-17 (hG-17) and the somatostatin analogue, desAA 1,2,4,5,12,13 [D-Trp8]somatostatin (ODT8-SS), significantly increased gastric acid secretion, while vasoactive intestinal peptide (VIP) had no effect. In the order of potency and efficacy, the following peptides decreased acid secretion: bombesin (BOM) greater than calcitonin gene-related peptide (CGRP) greater than calcitonin (CT) greater than corticotropin-releasing factor (CRF) greater than beta-endorphin (beta-END) greater than neurotensin (NT). In anesthetized rats, none of these peptides significantly altered proximal duodenal bicarbonate secretion. In awake, freely moving rats, cerebroventricular administration of CGRP significantly decreased while ODT8-SS, TRH and CRF significantly increased duodenal bicarbonate secretion. beta-Endorphin, VIP, CT, BOM, NT and hG-17 given i.c.v. did not significantly alter the bicarbonate response. These results indicate that neuropeptides administered into the central nervous system modulate gastric acid as well as duodenal bicarbonate secretions in awake, freely moving rats in a differentiated fashion. CGRP inhibits both acid and bicarbonate secretions, a somatostatin analogue and TRH both stimulate acid and bicarbonate secretions and CRF inhibits gastric acid but stimulates duodenal bicarbonate secretions.

Pathways mediating CRF-induced inhibition of gastric acid secretion in rats.

The pathways involved in mediating the central nervous system actions of corticotropin-releasing factor (CRF) on gastric acid secretion were examined in conscious rats. CRF (0.1-2.0 nmol) given cerebroventricularly inhibited gastric acid secretion stimulated by pentagastrin (P less than 0.01). This effect was abolished by cerebroventricular but not intravenous administration of a specific CRF receptor antagonist, alpha-helical CRF-(9-41). Ganglionic blockade with chlorisondamine chloride, noradrenergic blockade with bretylium, or adrenalectomy abolished the gastric inhibitory action of CRF whereas truncal vagotomy or opiate blockade with naloxone did not. A vasopressin receptor antagonist significantly inhibited but did not abolish the gastric inhibitory action of CRF. An intravenous infusion of epinephrine that mimicked the epinephrine plasma concentrations which were observed after cerebroventricular administration of CRF did not alter pentagastrin-stimulated gastric acid secretion. These results indicate that CRF acts within the central nervous system to inhibit gastric acid secretion by a specific receptor-mediated event. Inhibition of gastric acid secretion by CRF in conscious rats is mediated by efferent fibers of the sympathetic nervous system and in part by a vasopressin-dependent pathway but not by the parasympathetic nervous system, adrenal epinephrine release, or opiate-sensitive pathways.