1/10. 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.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
2/10. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema.BACKGROUND: Toxicity secondary to rectally administered hypertonic phosphate solution in patients with normal renal function is rarely reported in the literature. We report a case of electrolyte disturbance and seizure secondary to the rectal administration of 2 Fleet pediatric enemas. CASE REPORT: A 4-year-old white female with spinal muscular atrophy and chronic constipation was brought to the emergency department with complaints of lethargy and difficulty breathing following the administration of 2 Fleet pediatric enemas. In the emergency department, physical examination was significant for a depressed level of consciousness and shallow respirations. A basic metabolic profile was significant for a calcium of 3.3 mg/dL, phosphate of 23 mg/dL, and sodium of 153 mEq/L. Arterial blood gases revealed a pH of 7.24, Pco2 of 38 mm Hg, Po2 of 220 mm Hg. Electrocardiogram revealed a prolonged QT interval of 340 milliseconds with a corrected QT interval of 498 milliseconds. Sixteen hours postexposure, she experienced a generalized seizure unresponsive to multiple doses of lorazepam and responsive only to 100 mg of intravenous calcium chloride. Two days after presentation, the patient experienced complete resolution of symptoms. CONCLUSION: Osmotically acting hypertonic phosphate enemas can result in severe toxicity if retained. This is true even in patients without predisposing risk factors.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
3/10. Is there an upper limit of intracranial pressure in patients with severe head injury if cerebral perfusion pressure is maintained?Authors of recent studies have championed the importance of maintaining cerebral perfusion pressure (CPP) to prevent secondary brain injury following traumatic head injury. Data from these studies have provided little information regarding outcome following severe head injury in patients with an intracranial pressure (ICP) greater than 40 mm Hg, however, in July 1997 the authors instituted a protocol for the management of severe head injury in patients with a glasgow coma scale score lower than 9. The protocol was focused on resuscitation from acidosis, maintenance of a CPP greater than 60 mm Hg through whatever means necessary as well as elevation of the head of the bed, mannitol infusion, and ventriculostomy with cerebrospinal fluid drainage for control of ICP. Since the institution of this protocol, nine patients had a sustained ICP greater than 40 mm Hg for 2 or more hours, and five of these had an ICP greater than 75 mm Hg on insertion of the ICP monitor and later experienced herniation and expired within 24 hours. Because of the severe nature of the injuries demonstrated on computerized tomography scans and their physical examinations, these patients were not aggressively treated under this protocol. The authors vigorously attempted to maintain a CPP greater than 60 mm Hg with intensive fluid resuscitation and the administration of pressor agents in the four remaining patients who had developed an ICP higher than 40 mm Hg after placement of the ICP monitor. Two patients had an episodic ICP greater than 40 mm Hg for more than 36 hours, the third patient had an episodic ICP greater than of 50 mm Hg for more than 36 hours, and the fourth patient had an episodic ICP greater than 50 mm Hg for more than 48 hours. On discharge, all four patients were able to perform normal activities of daily living with minimal assistance and experience ongoing improvement. Data from this preliminary study indicate that intense, aggressive management of CPP can lead to good neurological outcomes despite extremely high ICP. Aggressive CPP therapy should be performed and maintained even though apparently lethal ICP levels may be present. Further study is needed to support these encouraging results.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
4/10. The electrocardiographic toxidrome: the ECG presentation of hydrofluoric acid ingestion.The clinician can approach the poisoned patient using the toxidrome system of toxin identification; this approach makes use of findings noted on the physical examination, highlighting the importance of abnormalities in blood pressure, heart rate, respiratory effort, body temperature, mental status, pupillary size, skin color, diaphoresis, and gastrointestinal sounds. Such a method provides structure and guidance to the clinical evaluation, providing the clinician with rapid diagnostic information and suggesting urgent management issues. A case of hydrofluoric acid poisoning is used as an example of this diagnostic approach. The patient demonstrated systemic toxicity accompanied by oral irritation and electrocardiographic abnormality (QRS complex widening and QT interval prolongation). The constellation of these findings suggested the possibility of a caustic agent (history and examination) with potential effect on potassium and calcium metabolism (electrocardiographic abnormalities). Such a constellation strongly suggested hydrofluoric acid as the culprit toxin.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
5/10. Haemodynamic instability during transhiatal resection of oesophagus results in postoperative metabolic acidosis and hypoxia: is there a need for assisted ventilation?Oesophagectomy for oesophageal carcinoma is a stressful physical and metabolic challenge for an individual. The metabolic acidosis and hypoxia resulting postoperatively in a 34-year-old male, suffering from oesophageal carcinoma, after transhiatal oesophagectomy was managed without assisted ventilation contrary to the usual teaching. Relevant literature has been reviewed.- - - - - - - - - - ranking = 0.07208123491431keywords = physical (Clic here for more details about this article) |
6/10. Episodes of severe metabolic acidosis in a patient with 3-methylglutaconic aciduria.Persistent excretion of 3-methylglutaconic acid was found in a 6-month-old infant with multiple minor physical malformations and delayed development. During two episodes of intercurrent viral illness, the patient developed severe metabolic acidosis and excreted large amounts of lactate, 3-hydroxybutyrate and acetoacetate. The excretion of 3-methylglutaconic acid did not change during these episodes, nor did it increase following leucine loading. in vitro studies suggest that in this patient, as in the majority of other patients with 3-methylglutaconic aciduria, a primary defect in leucine metabolism is not responsible for the biochemical abnormality.- - - - - - - - - - ranking = 0.07208123491431keywords = physical (Clic here for more details about this article) |
7/10. A variant form of 2-methyl-3-hydroxybutyric and 2-methylacetoacetic aciduria.A new case of assumed beta-ketothiolase deficiency, excreting 2-methyl-3-hydroxybutyrate and tiglylglycine is described in a 15-year-old boy. The patient presented with episodes of metabolic acidosis following intercurrent infections in the early childhood. After the age of 7 years he has had periods of headache, but no acidotic episodes have occurred even during infections. Systematic dietary treatment has not been instituted, and the patient is physically and mentally normal. This indicates a mild variant of the beta-ketothiolase deficiency. diagnosis of the condition may be obscured by large quantities of ordinary ketone bodies, and requires gas chromatographic and mass spectrometric techniques.- - - - - - - - - - ranking = 0.07208123491431keywords = physical (Clic here for more details about this article) |
8/10. Acid-base disorders: classification and management strategies.Acid-base disorders are common in clinical practice. Simple acid-base disturbances include metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis. Each can be clearly identified using a common clinical approach. Proper understanding of acid-base disorders requires knowledge of normal physiology. Each of the simple acid-base disorders can be diagnosed by obtaining a good history and performing a physical examination, followed by determinations of electrolyte levels, anion gap and pH. The degree and nature of compensation should then be analyzed. Finally, the ratio of the change in anion gap to the change in serum bicarbonate (delta AG/delta HCO3-) should be determined. When this diagnostic process is applied, proper identification of the disorder can be made and management can be undertaken. Mixed acid-base disorders can also be identified and managed using this method.- - - - - - - - - - ranking = 1keywords = physical examination, physical (Clic here for more details about this article) |
9/10. Transient glutamic acidaemia.We report on a severely hypotrophic male twin with persistent diarrhoea and metabolic acidosis during the first 4 weeks of life, who showed a fivefold normal glutamate concentration in plasma. Further evaluation excluded major defects in amino acid metabolism and after 5 months glutamate concentrations returned to normal. Neither the dizygotic twin sibling nor the parents revealed any clinical abnormalities or acid base or amino acid disturbances. Conclusion: Transient glutamic acidaemia seems to be an extremely rare condition in newborn infants and appears to be without negative impact on the physical and neurological development during the first months of life.- - - - - - - - - - ranking = 0.07208123491431keywords = physical (Clic here for more details about this article) |
10/10. Methylmalonic acidemia controlled with oral administration of vitamin B12.A 3-month-old male infant had two episodes of fever, projectile vomiting, dehydration, generalized fine tremors and gross metabloic ketoacidosis. methylmalonic acid was found in high concentration in both serum and urine, although the concentration of serum vitamin B12 was normal. A therapeutic trial of vitamin B12, administered parenterally, reduced greatly the methylmalonic aciduria. The patient has since been given vitamin B12 supplements continuously, initially 1 mg intramuscularly every other day, then 15 mg/d orally, and the protein in his diet was subsequently restricted. The most effected control of the methylmalonic aciduria was achieved with the combined regimen of oral vitamin therapy and dietary protein restriction. His physical and intellectual development have progressed normally and he has survived several acute respiratory tract infections without recurrence of metabolic acidosis.- - - - - - - - - - ranking = 0.07208123491431keywords = physical (Clic here for more details about this article) |
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