Cases reported "Acid-Base Imbalance"

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1/9. 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.
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2/9. diagnosis and treatment of an unusual cause of metabolic acidosis: ethylene glycol poisoning.

    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.
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3/9. 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.
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4/9. Arterial blood gases: clinical application.

    The interpretation of arterial blood gases (ABGs) is an essential assessment skill for the PACU nurse. ABG analysis can be fun and exciting, as well as an important tool for patient care. Acid-base imbalances are associated with various clinical conditions. Using ABGs as an assessment tool, the PACU nurse can determine the patient's acid-base status and initiate prompt, appropriate nursing intervention and medical consultation.
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5/9. Acid-base balance in real life panic.

    A case of naturally occurring panic attack is described. blood gas analysis was performed during and after the attack and compared with the baseline values in the same patient. The possible significance of the observed shifts is discussed.
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6/9. Respiratory failure.

    patients with respiratory failure should be approached in a systematic way, with emphasis both in diagnosis and treatment on arterial blood gases. The intelligent assessment of oxygenation, ventilation and acid-base balance, based on physiologic principles, can make the management of these patients very rewarding. The physiologic principles outlined here should be well understood by anyone entrusted with the care of these patients. They provide the cornerstone of diagnosis and management, and will remain valid long after current clinical dogma has been revised.
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7/9. Acid-base disturbance in patients with fulminant hepatic failure.

    Forty-two arterial blood pH and gas determinations were carried out on 11 patients with fulminant hepatic failure. The most common type of acid-base disturbance was that of respiratory alkalosis in 22 cases (52.4%). This was partially compensated in 13 subjects (31.0%) while an accompanying metabolic alkalosis was present in 9 (21.5%). Partially compensated metabolic acidosis was observed on 15 occasions (35.7%), all of which were in patients with laboratory evidence of impaired renal failure. The mental status of the patients was evaluated in each of the categories of acid-base disturbances. Some degree of correlation was evident between the PCO2 and the magnitude of base excess and that of the severity of the encephalopathy. The lower PCO2 and greater negative base excess values tended to be nearly always present in totally comatose subjects. By contrast, there was no clear cut relationship between pH and mental state.
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8/9. 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.
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9/9. Metabolic complications of the use of stomach for urinary reconstruction.

    A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.
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