A Degrading Potassium Tablet Mimicking Active Gastric Bleeding in a Computer Tomographic Investigation.

A 54-year-old male patient was admitted to the hospital due to symptoms caused by an intramural hematoma of the descending aorta. In a contrast media-enhanced computed tomography scan performed five days after admission to evaluate dynamics of the hematoma, a hyperdense lesion was seen in the stomach. A suspicion of gastric hemorrhage was raised at the first evaluation. Because the patient's clinical condition and hemoglobin levels were stable, gastroscopy to rule out an aorto-gastric fistula or another type of bleeding was not undertaken. In the secondary evaluation of the history and images, it became clear that the hyperdense lesion mimicking bleeding in the stomach must have been caused by a degrading potassium tablet ingested by the patient five hours before the investigation.

Muscle membrane dysfunction in critical illness myopathy assessed by velocity recovery cycles.

OBJECTIVE: To test the hypothesis that muscle fibers are depolarized in patients with critical illness myopathy by measuring velocity recovery cycles (VRCs) of muscle action potentials. METHODS: VRCs were recorded from brachioradialis muscle by direct muscle stimulation in 10 patients in intensive care with evidence of critical illness myopathy (CIM). Two sets of recordings were made, mean 3.9 d apart, and compared with those from 10 age-matched controls. RESULTS: Muscle supernormality was reduced in the patients by 50% compared with controls (P<0.002) and relative refractory period was increased by 59% (P<0.01). Supernormality was correlated with plasma potassium levels (R=-0.753, P<0.001), and the slope of this relationship was much steeper than previously reported for non-critically ill patients with renal failure (P<0.01). CONCLUSIONS: The abnormal excitability properties indicate that the muscle fibers in CIM were depolarized, and/or that sodium channel inactivation was increased. The heightened sensitivity to potassium is consistent with the hypothesis that an endotoxin reduces sodium channel availability in depolarized muscle fibers. SIGNIFICANCE: VRCs provide a practicable means to monitor muscle membrane changes in intensive care and to investigate the pathogenesis of CIM.

Oxygen extraction in pigs subjected to low-dose infusion of endotoxin after major abdominal surgery.

BACKGROUND: Sepsis may impair O(2) extraction due to blood flow redistribution or decreased utilization of the available oxygen. METHODS: We assessed the effect of endotoxemia on systemic and regional O(2) extraction and lactate handling in pigs, randomized to receive either endotoxin (0.4 microg kg(-1) h(-1); n = 10) or saline infusion (controls; n = 9) for 12 h. RESULTS: High baseline regional and systemic O(2) extraction in the endotoxin group (median 56%, range 45-77%) and in the controls (67%, 49-72%) was maintained until the end of the experiment (endotoxin group: 60%, 50-71%; controls: 60%, 50-74%) despite hypotension and a decrease in stroke volume in endotoxic animals. Hepatic lactate exchange decreased during endotoxemia from 14 micromol kg(-1) min(-1) (range 10-28 micromol kg(-1) min(-1)) to 10 (range 3-15) micromol kg(-1) min(-1); P < 0.01), but remained stable in the controls, with 13 micromol min(-1) (4-18 micromol min(-1)) at baseline and 7 micromol min(-1) (3-17 micromol min(-1)) after 12 h of saline infusion. CONCLUSIONS: The high and sustained oxygen consumption and oxygen extraction in this endotoxemic model speak against any major impairment of hepatosplanchnic or systemic oxygen extraction and oxidative metabolism. The reduced hepatic lactate exchange despite an unchanged hepatic lactate influx suggests altered metabolic activities independent of oxygen consumption.

Urinary iodine concentration during pregnancy in an area of unstable dietary iodine intake in Switzerland.

We prospectively investigated urinary iodine concentration (UIC) in pregnant women and in female, non-pregnant controls in the canton of Berne, Switzerland, in 1992. Mean UIC of pregnant women [205 +/- 151 microg iodine/g creatinine (microg l/g Cr); no. = 153] steadily decreased from the first (236 +/- 180 microg l/g Cr; no. = 31) to the third trimester (183 +/- 111 microg l/g Cr, p < 0.0001; no. = 66) and differed significantly from that of the control group (91 +/- 37 microg l/g Cr, p < 0.0001; no. = 119). UIC increased 2.6-fold from levels indicating mild iodine deficiency in controls to the first trimester, demonstrating that high UIC during early gestation does not necessarily reflect a sufficient iodine supply to the overall population. Pregnancy is accompanied by important alterations in the regulation of thyroid function and iodine metabolism. Increased renal iodine clearance during pregnancy may explain increased UIC during early gestation, whereas increased thyroidal iodine clearance as well as the iodine shift from the maternal circulation to the growing fetal-placental unit, which both tend to lower the circulating serum levels of inorganic iodide, probably are the causes of the continuous decrease of UIC over the course of pregnancy. Mean UIC in our control group, as well as in one parallel and several consecutive investigations in the same region in the 1990s, was found to be below the actually recommended threshold, indicating a new tendency towards mild to moderate iodine deficiency. As salt is the main source of dietary iodine in Switzerland, its iodine concentration was therefore increased nationwide in 1998 for the fourth time, following increases in 1922, 1965 and 1980.

Heart and brain: a case of focal myocytolysis in severe pneumococcal meningoencephalitis with review of the contemporary literature.

We report electrocardiographic changes mimicking myocardial ischaemia in a 73-year-old man with fatal pneumococcal meningoencephalitis, present the autopsy-confirmed histological picture of extensive focal myocytolysis (contraction band necrosis) without myocardial infarction or myocarditis, and review the contemporary literature. Potentially reversible, probably non-ischaemic myocardial dysfunction may occur in association with acute noncardiac illnesses, such as brain injuries. Biochemical and morphological abnormalities in acutely failing hearts from head-injured organ donors point to specific pathophysiological mechanisms, which are different from heart failure from other causes. Sepsis-related factors may add to the myocardial dysfunction in patients with brain injury from meningoencephalitis.

Continuous left hemidiaphragm sign revisited: a case of spontaneous pneumopericardium and literature review.

In pneumopericardium, a rare but potentially life threatening differential diagnosis of chest pain with a broad variety of causes, rapid diagnosis and adequate treatment are crucial. In upright posteroanterior chest radiography, the apical limit of a radiolucent rim, outlining both the left ventricle and the right atrium, lies at the level of the pulmonary artery and ascending aorta, reflecting the anatomical limits of the pericardium. The band of gas surrounding the heart may outline the normally invisible parts of the diaphragm, producing the continuous left hemidiaphragm sign in an upright lateral chest radiograph. If haemodynamic conditions are stable, the underlying condition should be treated and the patient should be monitored closely. Acute haemodynamic deterioration should prompt rapid further investigation and cardiac tamponade must be actively ruled out. Spontaneous pneumopericardium in a 20 year old man is presented, and its pathophysiology described.

[Iodine-induced hyperthyroidism (iodine-induced Basedow's disease): a current disease picture]. / Die Jod-induzierte Hyperthyreose (Jodbasedow): ein aktuelles Krankheitsbild.

Iodine-induced thyrotoxicosis or "jodbasedow phenomenon" has been reported throughout the world since iodine has been administered to treat endemic goitre. Nowadays, iodinated radiocontrast agents and the antiarrhythmic drug amiodarone are the most common sources of excess iodine load subsequently leading to iodine-induced thyrotoxicosis, especially in elderly patients with underlying goitre. The aim of the study was to identify the number of cases of iodine-induced thyrotoxicosis among patients with thyrotoxicosis in a large urban hospital. Over an 18-month period thyrotoxicosis has been diagnosed in a total of 39 patients. Eight patients with iodine-induced thyrotoxicosis (5 female, 3 male; mean age 60.6 years) have been identified (20%). In all patients with iodine-induced thyrotoxicosis, iodine exposure with a mean iodine dose of 21.5 g was documented 2 to 16 weeks before diagnosis (iodinated radiocontrast agents in 5 patients, amiodarone in 2 patients, kelp tablets in 1 patient). Clinical features were predominantly tachyarrhythmias and heart failure, while 6 of 8 patients had goitre (thyroid volume 31 to 193 ml). Thyroid antibodies were not detected. Diagnosis was confirmed in 5 of 8 patients with increased urinary iodine concentrations (3436 to > 6000 nmol/24 h), and in 3 of 8 patients with a low tracer uptake in thyroid scintigraphy (1 to 4%). Treatment consisted of methimazole in all patients, additional tional beta-blockers and lithium in 4 patients, and prednisone in 5 patients. The mean treatment ment duration was 9.2 months, and patients became euthyroid after a mean treatment duration of 6.4 weeks. One patient (with still elevated free thyroxine levels) died of myocardial infarction 4 weeks after antithyroid drug therapy had been installed. The incidence, mechanisms and features of iodine-induced thyrotoxicosis are discussed. Iodine-induced thyrotoxicosis is a common disease, and the recognition and treatment of iodine-induced thyrotoxicosis, particularly in elderly patients and patients with goitre, are of clinical importance.

[Why is iodine deficiency once again present in the Berne region?]. / Warum besteht erneut und noch immer Jodmangel in der Region Bern?

Owing to the progressive iodination of salt in Switzerland (5, 10, 20 mg KI/kg in the years 1922, 1965, 1980), iodine deficiency in former endemic goiter regions had nearly disappeared. In several areas of the country, urinary iodine had increased from below 30 micrograms/24 h (1920) to > 100 micrograms/g creatinine (1981-1990). In 1991-1992, however, the 24-h-iodinuria in a subgroup of 160 examinations out of a total of 289 persons in Berne was again insufficient (norm > 150 micrograms J/24 h): mean 121 micrograms/24 h (82 micrograms/l), median 107.8 micrograms/24 h (67 micrograms/l). Follow-up of one proband in 1991-1992 (n = 9) and 1996 (n = 11) yielded average 24-h-iodinurias in the slightly deficient domain of (mean +/- SD) 104 +/- 57 micrograms/ 24 h (75 +/- 30 micrograms/l) and 103 +/- 27 micrograms/24 h (44 +/- 17 micrograms/l) respectively, with a wide range (45-258 micrograms l/24 h globally). Possible reasons for the decreasing iodide intake in recent years, resulting in the 1990s in a marginally deficient supply, are reduced intake of salt in recent decades, increased consumption of foodstuffs prepared with non-iodized salt, dietary diversification, and frequent meals away from the family table. Therefore, intake of non-iodized salt should be avoided in Switzerland.

The instability of dietary iodine supply over time in an affluent society.

In the Bernese region, where goiter was formerly endemic, alimentary salt has been supplemented by increasing amounts of potassium iodide (KI): 5, 10, 20 mg KI/kg in 1922, 1965 and 1980 respectively. Ioduria rose from < 30 micrograms I/g creatinine in 1920 to > 100 micrograms I/g creatinine in the 1980s. In 1992 ioduria was estimated in 55 healthy volunteers (group A and individual B) and 234 thyroid carcinoma patients after thyroidectomy: hypothyroid patients with (C) and without thyroid remnants (D) and euthyroid patients on T4 substitution (E). The arithmetic mean iodine excretion of the healthy volunteers in group A and individual B was found to be 87 +/- 40 micrograms I/g creatinine. This is insufficient according to the recommendations of the WHO. In all groups, the iodine excretion reached the recommended level only in some members: 24% (A, B), 19% (C), 38% (D) and 81% (E). It was thought in the 1980s that in a formerly iodine-deficient society, iodinated salt would continue to provide an adequate supply of iodine. However, iodine intake in this affluent society has proved to be unstable. This can be attributed to modifications of eating habits, which include a reduction of total salt consumption, combined with a growing consumption of manufactured food of cosmopolitan origin, prepared using salt containing little or no iodine.