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Acquired Stomatocytosis in Hyperosmolar Hyperglycemic Derangement Abstract. In the context of a suicidally motivated suspension of insulin therapy, a massive hyperosmolar hyperglycemic derailment occurred in pancreoprivic diabetes mellitus most likely due to aethyltoxicity. In the blood picture differentiation stomatocytes could be detected, the development of which will be discussed in more detail below.

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Rare Complication of a Common Disease: Thyroid and Epileptic Seizures Abstract. A myxedema crisis is a life-threatening complication of hypothyroidism (mortality 20-25 %). The diagnosis is made on clinical grounds and thyroid function tests. Treatment with levothyroxine (possibly combined with T3) should be instituted immediately, along with glucocorticoids, until co-existing adrenal insufficiency has been ruled out. Supportive measures and treatment of underlying diseases should be implemented. We are presenting the case of a patient with myxedema crisis complicated by tonic-clonic seizures and severe hyponatremia as first manifestation of primary hypothyroidism.

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A patient with a history of metastatic bronchial carcinoma and end stage heart disease was admitted to hospital, after an accidental fall, because of epistaxis requiring nasal tamponade and blood transfusions. On day 2 the patient suffered from acute dyspnoea and finally respiratory and cardiac arrest. The patient was successfully resuscitated despite a do not resuscitate order (DNR order). A bolus aspiration of the nasal tamponade's gauze was discovered as the reason for the arrest. This case report underlines the ethical dilemma in patients with an otherwise undisputed DNR order when the arrest is: (1) easy to resolve but not easy to detect; (2) iatrogenic in nature; and (3) is occurring in an unmonitored area (for example, the ward) as compared with an arrest in a well monitored area (for example, the intensive care unit and operating room).

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INTRODUCTION: The effect of expiratory endotracheal tube (ETT) resistance on dynamic lung inflation is unknown. We hypothesized that ETT resistance causes dynamic lung hyperinflation by impeding lung emptying. We further hypothesized that compensation for expiratory ETT resistance by automatic tube compensation (ATC) attenuates dynamic lung hyperinflation. METHODS: A ventilator equipped with the original ATC mode and operating in a pressure-targeted mode was connected to a physical lung model that consists of four equally sized glass bottles filled with copper wool. Inspiratory pressure, peak expiratory flow, trapped lung volume and intrinsic positive end-expiratory pressure (PEEP) were assessed at combinations of four inner ETT diameters (7.0, 7.5, 8.0 and 8.5 mm), four respiratory rates (15, 20, 25 and 30/minute), three inspiratory pressures (3.0, 4.5 and 6.0 cmH2O) and four lung compliances (113, 86, 58 and 28 ml/cmH2O). Intrinsic PEEP was measured at the end of an expiratory hold manoeuvre. RESULTS: At a given test lung compliance, inspiratory pressure and ETT size, increasing respiratory rates from 15 to 30/minutes had the following effects: inspiratory tidal volume and peak expiratory flow were decreased by means of 25% (range 0% to 51%) and 11% (8% to 12%), respectively; and trapped lung volume and intrinsic PEEP were increased by means of 25% (0% to 51%) and 26% (5% to 45%), respectively (all P < 0.025). At otherwise identical baseline conditions, introduction of expiratory ATC significantly attenuated (P < 0.025), by approximately 50%, the respiratory rate-dependent decreases in inspiratory tidal volume and the increases in trapped lung volume and intrinsic PEEP. CONCLUSIONS: In a lung model of pressure-targeted ventilation, expiratory ETT resistance caused dynamic lung hyperinflation during increases in respiratory rates, thereby reducing inspiratory tidal volume. Expiratory ATC attenuated these adverse effects.

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We report the case of attempted suicide with amlodipine, chlorthalidone and mefenamic acid and subsequent medical intensive care measures which resulted in total recovery of a 42-year-old male. After admission to the medical intensive care unit the intoxicated patient was deeply hypotensive and needed fluid replacement, dobutamine and norepinephrine. Additionally insulin and calcium gluconate were given. Since hypotension persisted and the patient developed oliguria, terlipressin was applied and finally showed an effect on blood pressure and on urinary output. A volume overload of 7 L in the first 24 h resulted in a pulmonary edema. The patient was started on non-invasive ventilation with continuous positive airway pressure (CPAP) and frusemide was added to the therapy with good success. Quantitative determination of amlodipine in plasma samples was performed by liquid chromatography-tandem mass spectrometry (LC-MS/MS). The highest amlodipine concentrations was measured in the plasma sample collected approximately 8 h after ingestion of the drug, and was 393 microg/L. Four days later, it was possible to stop the treatment with catecholamines, at that time the amlodipine plasma concentration had declined to 132 microg/L, still tenfold higher than therapeutic (5-18 microg/L). Elimination half-life of amlodipine is approximately 55 h. After 6 days in the intensive care unit the patient was transferred to psychiatric treatment. Intensive care management and plasma levels in this intoxication case are compared to data from literature on other cases.

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