1/49. pH-dependent cocaine-induced cardiotoxicity. Severe cocaine toxicity causes acidemia and cardiac dysfunction. These manifestations are described in 4 patients who presented with seizures, psychomotor agitation, and cardiopulmonary arrest. Their initial laboratory values demonstrated acidemia and electrocardiographic findings that included a prolonged QRS complex and QTc duration and a rightward T40 ms axis deviation. Treatment of the patients with hyperventilation, sedation, active cooling, and sodium bicarbonate infusion led to the normalization of their blood pHs and reversal of their cardiac conduction disorders. Acidemia can contribute to cocaine cardiac disorders by promoting conduction delays, dysrhythmias, and depressed myocardial contractility. Good supportive care corrects the blood pH and cardiac conduction disorders and remains the major focus in the management of patients with cocaine toxicity. ( info) |
2/49. Gastric intramucosal pH as a monitor of gut perfusion after thrombosis of the superior mesenteric vein. Gastric intramucosal pH (pHi) when measured by a tonometer is a simple and minimally invasive method to determine gut ischemia. In a case of severe mesenteric venous thrombosis, we measured pHi intra- and postoperatively over a period of five days. The goal was to monitor improvement or deterioration of gastrointestinal perfusion in the intensive care unit and to perform a second-look laparotomy if the condition worsened. We observed that gastric pHi is a more sensitive parameter for detecting intestinal ischemia than parameters such as arterial pH, base excess, or lactate. This patient's pHi rose continuously, which allowed us to proceed in a conservative way without any further invasive diagnostic interventions. Thus, the application of a gastric tonometer in cases of mesenteric venous thrombosis may help to reduce costs by preventing unnecessary postoperative diagnostic maneuvers such as angiography, computed tomography, or even second-look laparotomy. ( info) |
| ethylene glycol intoxication is a rare but dangerous type of poisoning. It causes a severe acidosis with high anion and osmolal gaps. Clinical manifestations of the ethylene glycol intoxication can be divided in three phases: a neurologic stage, with hallucinations, stupor and coma; the second stage is cardiovascular with cardiac failure. Renal failure characterizes the third stage, due to acute tubular necrosis. After aggressive gastric emptying, the main treatment is ethanol or 4-methypyrazole, which can be given either orally or intravenous, with supportive measures for all symptoms or diseased organ. ( info) |
4/49. A stepwise approach to acid-base disorders. Practical patient evaluation for metabolic acidosis and other conditions. Acid-base disorders can usually be approached by following the steps outlined in the text and doing the calculations shown in the box on page 257. Clues about the underlying disorder can be obtained from history taking and physical examination. Assessment of pH, PaCO2, and HCO3- allows determination of whether a primary metabolic or respiratory disorder is present. Calculation of the predicted compensatory response for simple acid-base disorders might suggest the presence of an additional disease process if compensation is not appropriate. Calculation of the various gaps can be helpful in differential diagnosis (i.e., anion gap for diagnosis of metabolic acidosis, delta anion gap for diagnosis of high-anion-gap metabolic acidosis, and urine anion gap for diagnosis of a non-anion gap metabolic acidosis). Most acid-base problems can be solved with use of the stepwise approach described. ( info) |
5/49. The diagnosis of brain depression in the presence of severe multisystem disease--a case study. Brain depression in a patient with severe multisystem disease can be a diagnostic challenge, particularly when the patient is maintained on artificial life-support systems. A case report is presented of a 13-year-old girl with severe pneumonia who was treated with prolonged cardiopulmonary bypass during which time she developed a clinical picture simulating brain death with marked depression of cerebral cortical activity on two successive EEGs. Following correction of some of her metabolic defects, the patient showed marked improvement of cortical function. Multisystem disease can be so severe as to produce a clinical picture of brain death. We wish to emphasize that brain hypofunction of depression is best evaluated by both clinical examination and the EEG, and that neither one alone is sufficient to conclude that cerebral death has occurred. ( info) |
6/49. Reduced Tc-99m DMSA uptake in a patient with renal tubular acidosis: effect of acid-base imbalance. Tc-99m dimercaptosuccinic acid (DMSA) is used as a renal cortical imaging agent to detect parenchymal abnormalities especially in children. kidney uptake of DMSA provides an index for evaluation of a functional tubular mass, which depends on the renal blood flow and proximal tubular cell membrane transport function. We here report a boy with renal tubular acidosis, which has noticeably reduced uptake on his Tc-99m DMSA scintigraphy, despite a totally normal Tc-99m MAG-3 study. The case reported here clearly demonstrates a situation in which renal uptake of DMSA may be dissociated from a functional renal mass and the importance of acid-base balance which alters Tc-99m DMSA uptake. ( info) |
7/49. 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. ( info) |
| This is the first case reported of vomiting-induced metabolic alkalosis associated with myoclonus. The report describes an unusual presentation of myoclonus secondary to acid-base disturbance caused by recreational drug-induced vomiting. The severe derangement of hyponatraemia, hypokalaemia, and alkalosis appears to have been reasonably well tolerated due to the gradual onset and relatively long history. The causes, mechanism, and management of metabolic alkalosis are discussed. ( info) |
9/49. 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. ( info) |
| refeeding syndrome is a very serious disorder that is not often observed today, as it is more common during times of mass starvation or war. Nowadays, it is sometimes found in patients suffering from anorexia nervosa or neoplastic diseases. A case recently treated in our intensive care Unit is described. The patient was pregnant and suffering from Crohn's disease. It is emphasized that although refeeding syndrome is often fatal if not treated early, it is easily prevented or treated with adequate nutritional support. ( info) |