Risk stratification of early admission to the intensive care unit of patients with no major criteria of severe community-acquired pneumonia: development of an international prediction rule. Serum lactate as a predictor of mortality in emergency department patients with infection. Ann Emerg Med. Lactate measurements in sepsis-induced tissue hypoperfusion: results from the Surviving Sepsis Campaign database. Serum lactate upon emergency department arrival as a predictor of day in-hospital mortality in an unselected population.
Prognostic value of incremental lactate elevations in emergency department patients with suspected infection. Comparison of the prognostic significance of initial blood lactate and base deficit in trauma patients. Prognostic significance of blood lactate and lactate clearance in trauma patients. Lactate level versus lactate clearance for predicting mortality in patients with septic shock defined by sepsis Failure to clear elevated lactate predicts hour mortality in trauma patients.
Resource utilization in treatment of diabetic ketoacidosis in adults. Am J Med Sci. Moss JM. Diabetic ketoacidosis: effective low-cost treatment in a community hospital. South Med J. Marinac JS, Mesa L.
Using a severity of illness scoring system to assess intensive care unit admissions for diabetic ketoacidosis. Variation in use of intensive care for adults with diabetic ketoacidosis. Subcutaneous rapid-acting insulin analogues for diabetic ketoacidosis.
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Am J Med. Treatment of diabetic ketoacidosis with subcutaneous insulin aspart. Managing diabetic ketoacidosis in non-intensive care unit setting: role of insulin analogs. Indian J Pharmacol. Is a priming dose of insulin necessary in a low-dose insulin protocol for the treatment of diabetic ketoacidosis? Utility of initial bolus insulin in the treatment of diabetic ketoacidosis.
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Lancet Lond Engl. The effects of sodium bicarbonate during prolonged cardiopulmonary resuscitation. Prehospital sodium bicarbonate use could worsen long term survival with favorable neurological recovery among patients with out-of-hospital cardiac arrest. Sodium bicarbonate administration during ongoing resuscitation is associated with increased return of spontaneous circulation. The effects of calcium and sodium bicarbonate on severe hyperkalaemia during cardiopulmonary resuscitation: a retrospective cohort study of adult in-hospital cardiac arrest.
Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation. Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest. European resuscitation council guidelines for resuscitation section 1.
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New York: Elsevier; Quantitative cerebrospinal fluid acid—base balance in acute respiratory alkalosis. Ventilatory drive in acute metabolic acidosis. J Appl Physiol. Ventilatory response in patients with acute lactic acidosis. Acidosis in the critically ill—balancing risks and benefits to optimize outcome. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: Effects of clinically relevant acute hypercapnic and metabolic acidosis on the cardiovascular system: an experimental porcine study.
Mechanical ventilation to minimize progression of lung injury in acute respiratory failure. Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study. Download references. You can also search for this author in PubMed Google Scholar. All authors provided references. All authors read and approved the final manuscript. Correspondence to Boris Jung. The authors declare the following competing interests: B. Jung: Sedana Medical, Medtronic; M. Terzi: Boehringer Ingelheim, Pfizer; D.
Viglino: Astra Zeneca, Mundipharma; Y. The remaining authors declare that they have no competing interests. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and Permissions. Jung, B. Diagnosis and management of metabolic acidosis: guidelines from a French expert panel. Intensive Care 9, 92 Download citation. Received : 26 June Accepted : 30 July Published : 15 August Anyone you share the following link with will be able to read this content:.
Variation of symptoms 3. Lack of clinical experience 4. Lack of diagnostic equipment 5. Limited availability of treatment options 6. High morbidity and mortality. Methanol and formaldehyde poisoning. In: Brent J al eds. Critical Care Toxicology, 2 nd Edition. Springer Publishing. Online Early. Scand J Clin Lab Invest ; 75 7 : Asymptomatic patients: Observe.
Hyperventilation, no visual disturbances. Observe minimum 24 hours C. Hyperventilation, visual disturbances, conscious: Give ethanol, bicarbonate, folinic acid, consider transport to dialysis facilities D. Hyperventilating, unconscious: Give ethanol in an oral tube , bicarbonate, folinic acid, transport to dialysis facilities E. Avoid ethanol in case this is a ethanol intoxication instead unless confident on diagnosis.
Give bicarbonate, folinic acid and consider transferral if possible. Clin Toxicol ; 2 Hovda KE et al. Clin Tox ; 7 Zakharov et al. Clin Tox ; Simplified treatment protocols. All of theaboveshould beinitiated asearly aspossible,but any of thesetreatmentsareimportant — Usewhat you haveavailable! Criterion for treatment when methanol poisoning is suspected clinical findings only : A. Reevaluate in two hours Make new plan based on the new data Correct the underlying cause s.
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Description: ppt file. Flag for inappropriate content. Download now. Related titles. Carousel Previous Carousel Next. Jump to Page. Search inside document. Any calculated amount is approximate Fernandez et al have derived a formula for calculating the bicarbonate space KI , 0. Eric Chye Teck. Total oxidation of acetoacetate is the principal metabolic fate in normal m a n and may be represented as CHACO. Accumulation of ketone bodies due to an imbalance between production and utilization rates occurs in normal man during starvation and in uncon- trolled diabetes mellitus.
Under controlled conditions Miles and colleagues withheld insulin therapy from insulin-dependent diabetics for ten hours. Ketone b o d y production increased from 5. At the end o f ten hours of insulin deprivation, the net accumulation o f ketone bodies in the body was therefore 3. P r o f o u n d acidosis and acidaemia must, therefore, result unless ketone body production decreases or utilization rises. In a similar fashion, 4 A T P are expended in the conversion of glucose itself to lactate and back, and 1 A T P and 1 UTP in the interconversion of glycogen and glucose.
Other cycles may be more complex, such as that between triglyceride and fatty acids. New glycerol 3-phosphate is necessary for tripalmitoyl glycerol synthesis. In liver, this may arise directly from glycerol, requiring one molecule o f A T P , whereas in adipose tissue glycerol phosphate must be formed from glucose also requiring 1 ATP.
The formation of glycerol 3-phosphate from dihydroxyacetone phosphate utilizes one molecule o f reduced NAD. This might otherwise have been utilized for the synthesis of 2 A T P so we shall not include this in the calculation. Glucose metabolism to lactate, pyruvate or alanine and back accounts for 12 per cent of total glucose turnover, while the extent o f other forms o f substrate cycling in glycolysis is unknown in man. In vitro studies with rat adipose tissue suggest that much of the fatty acid released may be reincorporated into triglyceride Steinberg and Vaughan, ; May, This is exemplified by triglyceride hydrolysis in adipose tissue with release o f non-esterified fatty acid NEFA which may be reincorporated into triglyceride in the liver.
Little information is available on the rates o f substrate cycling in disease states in man, although thyroid hormone excess induces an increase in glucose cycling to 3-carbon inter- mediates McCulloch et al, A notable exception is the oxidation o f sulphur- containing amino acids Lemann and Relman, The oxidation o f methionine, cysteine or homocysteine involves initial conversion of sulphydryl groups to sulphinate, then sulphite, and finally sulphate groups which are excreted in the urine with ammonium.
Similarly the hydrolysis of phosphoester groups in phosphoproteins and also in phospholipids and nucleic acids generates phosphoric acid Lennon, Lemann and Relman, The principal determinant of a low urine pH, under normal conditions, is the quantity o f sulphur-containing amino acid oxidized to sulphate, and o f phosphorus- containing compounds oxidized to phosphoric acid. A high intake of these acids, even from large quantities o f fruit and vegetables, does not result in significant acidaemia.
Within the circulation CO2 is transported in a variety of ways. Approximately 7 per cent o f that produced is transported in the dissolved state, while a further per cent is bound to protein.
Haemoglobin is the major protein concerned and the amount o f carbaminohaemoglobin produced is inversely related to the degree of haemoglobin saturation with oxygen the Haldane effect. These processes are reversed equally rapidly in the lungs as COs is lost from the circulation to alveolar air.
The excretion o f volatile acid is thus achieved purely by respiratory means. A m i n o acids, particularly histidine, and proteins constitute a m a j o r intracellular buffer, and approximately 60 per cent of the buffering capacity of muscle Rahn, Reeves and Howell, ; Sahlin, Intracellular bicarbonate constitutes the bulk of the remainder, approximately per cent in muscle tissue.
A body deficit of H C O 3- remains which must be restored by the kidneys. The m a j o r extracellular buffers are the bicarbonate system, protein and inorganic phosphate, with bicarbonate the most important Table 2 Schwartz, Orning and Porter, ; Cohen, Table 2. The breakdown of intracellular buffers is that for muscle tissue Jones, The vascular compartment accounted for 18 per cent of the total buffer, mostly plasma HCO3- and erythrocyte haemoglobin.
Minute ventilation varies with the CSF or arterial pH determined by central medullary or carotid body chemoreceptors respectively. Under normal circumstances, the central medullary respiratory centre is the more important. The ventilatory response involves an increase in both tidal voiume and in respiratory rate to eliminate CO2 as pH falls, and vice versa. The p H reduction which stimulates the chemoreceptors in acidoses may arise as a consequence of a primary increase in CO2 or a decrease in bicarbonate.
An increase in respiration will completely normalize the abnormality in the former case of a respiratory acidosis, whereas in the latter metabolic acidosis, the respiratory response is purely compensatory and bicarbonate must be regenerated by other means. The maximum reduc- tion in pCO2 which may be achieved by increased ventilation in severe metabolic acidosis is to between 15 and 20 mm Hg.
This is not a universal finding, however, and in other studies the arterial pC02 was appropriately decreased throughout the p H range Fulop, , This removes the small amounts o f acid generated from metabolism o f sulphur and phosphorus-containing compounds, uric acid and creatinine excretion and excretion o f minor amounts of other organic acids, particularly the ketone bodies, which occurs under normal circumstances.
Under normal circumstances almost all the filtered bicarbonate is reabsorbed with sodium in the proximal tubule. This process is increased by volume expansion, a high p C O 2 and hypokalaemia O ' C o n n o r and Kunau, , but is not responsible for the generation of additional H C O a- to replace that lost during the development o f a metabolic acidosis.
This distal acid secretion occurs in association with sodium reabsorption, so that factors which increase the delivery of sodium to the distal nephron increase this process. Other factors such as hypokalaemia have the same effect, but the principal modulator in the present context is the effect of acidosis to increase renal ammonia synthesis and ammonium ion excretion. A tenfold increase in ammonium excretion may occur after systemic acidosis lasting days.
Glutamine is the major source of nitrogen for ammonium production under the influence of the enzyme glutaminase. Additional systemic alkalinization may be obtained as the carbon skeleton o f glutamine is oxidized with the generation o f bicarbonate Oliver and Bourke, The glutamine required for ammonia synthesis derives from muscle and is transported to the kidneys in the plasma.
Muscle glutamine release increases in acidosis Schr0ck and Goldstein, as does renal uptake Parry and Brosnan, In consequence, plasma glutamine concentrations in chronically acidotic man may be decreased or normal Owen and Robinson, ; Tizianello et al, In chronic acidosis, transport of glutamine into renal cells and across the mitochondrial membrane for metabolism is increased, as is the activity o f the enzyme glutaminase Tannen, ; Alleyne et al, , for reviews.
These m a y be charac- terized by excessive acid production, diminished metabolism or excretion of acid, or a combination o f these mechanisms. Diabetic ketoacidosis exhibits several of these mechanisms. The primary abnormality is excessive production o f ketone bodies coupled to an impair- ment of ketone b o d y utilization, both consequent upon absolute or relative insulin deficiency. Finally, some patients have a secondary lactic acidosis which contributes to the acidaemia and acidosis.
Production o f acid in excess of the capacity for its utilization occurs also in Type A and Type B lactic acidosis. In Type A the acidosis accompanies shock, hypotension and hypoxia, and large amounts of lactic acid are produced by tissues with a high glycolytic capacity as a result o f anoxia.
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