1/5. An unusual cause of hypokalemic paralysis: chronic licorice ingestion.Long-term licorice ingestion is a well-known cause of secondary hypertension and hypokalemia. Nevertheless, its initial presentation with a very severe degree of hypokalemia and paralysis is exceedingly rare. We report an elderly Asian man who presented to the emergency department with marked muscle weakness that progressed to paralysis. His blood pressure was 160/96 mm Hg. The major biochemical abnormalities were hypokalemia (plasma K concentration, 1.8 mmol/L) and metabolic alkalosis (HCO - 3 , 36 mmol/L). His renal potassium excretion was higher (transtubular potassium gradient of 9). plasma renin activity and aldosterone concentration were suppressed and cortisol concentration was normal. A detailed history revealed that he had ingested tea flavored with 100 g of natural licorice root containing 2.3% glycyrrhizic acid daily for 3 years. Note that renal potassium wasting and hypertension persisted for 2 weeks after discontinuing licorice consumption along with KCl supplement and spironolactone. Long-term licorice ingestion should be kept in mind as a cause of paralysis with an extreme degree of hypokalemia to avoid missing this recognizable and curable medical disorder.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
2/5. Dynamic changes in regional CBF, intraventricular pressure, CSF pH and lactate levels during the acute phase of head injury.The authors measured regional cerebral 133xenon (133Xe) blood flow (rCBF), intraventricular pressure (IVP), cerebrospinal fluid (CSF) pH and lactate, systemic arterial blood pressure (SAP), and arterial blood gases during the acute phase in 23 comatose patients with severe head injuries. The IVP was kept below 45 mm Hg. The rCBF was measured repeatedly, and the response to induced hypertension and hyperventilation was tested. Most patients had reduced rCBF. No correlation was found between average CBF and clinical condition, and neither global nor regional ischemia contributed significantly to the reduced brain function. No correlation was found between CBF and IVP or CBF and cerebral perfusion pressure (CPP). The CSF lactate was elevated significantly in patients with brain-stem lesions, but not in patients with "pure" cortical lesiosn. The 133Xe clearance curves from areas of severe cortical lesions had very fast initial components called tissue peaks. The tissue peak areas correlated with areas of early veins in the angiograms, indicating a state of relative hyperemia, referred to as tissue-peak hyperemia. Tissue-peak hyperemia was found in all patients with cortical laceration or severe contusion but not in patients with brain-stem lesions without such cortical lesions. The peaks increased in number during clinical deterioration and disappeared during improvement. They could be provoked by induced hypertension and disappeared during hyperventilation. The changes in the tissue-peak areas appeared to be related to the clinical course of the cortical lesion.- - - - - - - - - - ranking = 7keywords = pressure (Clic here for more details about this article) |
3/5. Pathogenesis of acidosis in hereditary fructose intolerance.An 18-yr-old man with a classical history of hereditary fructose intolerance (HFI) developed typical biochemical changes following an oral fructose load: fructosemia, hypoglycemia, hypophosphatemia, hyperuricemia, and metabolic acidosis. hypokalemia (3.1 meq/liter) was also noted. Three aspects of this case expand the published literature on this syndrome: (1) Metabolic acidosis was found to be due to both lactic acidosis and proximal renal tubular acidosis (RTA). We could quantitate the relative contribution of each, and found that urinary bicarbonate loss due to proximal RTA accounted for less than 10% of the fall in serum bicarbonate. The major cause of the metabolic acidosis was lactic acidosis. (2) hypokalemia was found to be due to movement of potassium out of the extracellular space rather than to urinary loss. potassium may have entered cells with phosphate or may have been sequestered in the gastrointestinal tract. (3) The coexistence of proximal RTA and acidemia made it possible to study the effect of acidemia on the urine-blood partial pressure of carbon dioxide (PCO2) gradient in alkaline urine (U-B PCO2). The U-B PCO2 measured during acidemia was much higher at the same urine bicarbonate concentration than in normal controls during alkalemia, providing evidence in humans that acidemia stimulates distal nephron hydrogen-ion secretion.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |
4/5. MAST: medical antishock trousers.MAST are a simple, safe and sound device with applicability in all shock states; they provide a number of benefits to the hypotensive patient. The main benefits seem to be autotransfusion of peripherally pooled blood originating from the MAST encased areas, increase in peripheral vascular resistance, external tamponade of bleeding vessels and an aid to stabilization of fractured bones of the pelvis and lower extremities. Because an area of hypoperfusion can lead to complications, the pathophysiologic effects of MAST must be understood. The greatest complications occur when MAST are too rapidly removed. They must be removed in an appropriate place by trained physicians under controlled conditions. The key is to deflate the MAST over a prolonged period of time using a gradual release of external pressure. Volume status and acid-base balance must be carefully monitored. In the last few years MAST have had an ever expanding role in both the pre-hospital and hospital phases of care of the critically ill and injured patients. All physicians involved in the care of these patients must be familiar with this device. Applied and removed properly, MAST will sustain blood pressure and save lives.- - - - - - - - - - ranking = 2keywords = pressure (Clic here for more details about this article) |
5/5. A re-appraisal of the tri-axial chart for monitoring arterial acid-base values.OBJECTIVE: To demonstrate the practicability of a tri-axial chart for the graphical and quantitative monitoring of arterial pH, arterial carbon dioxide partial pressure (PaCO2) and actual arterial bicarbonate-ion concentration (a[HCO3-]) in intensive care patients. DESIGN: Case report. SETTING: A general intensive care unit (ICU). methods: Using a standard mathematical transformation, a data set of pH, log PaCO2 and log a[HCO3-] values can be transformed in such a way that a graphical display of all three variables is possible while being faithful to their linear relationship. Remarkably, the graphical display closely resembles the tri-axial chart that Hastings and Steinhaus described in 1931 for studying displacements of the acid-base balance. Two new monitoring parameters based on the chart and the transformation are described. One monitors the abnormality of the acid-base status while the other monitors the rate of acid-base changes. CONCLUSIONS: With the tri-axial acid-base chart, the complete acid-base status can be faithfully monitored. Moreover, the proposed monitoring parameters provide extra information about the arterial acid-base status that, otherwise, would remain hidden.- - - - - - - - - - ranking = 1keywords = pressure (Clic here for more details about this article) |