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Thread: Patient w/ Diabetic Ketoacidosis

  1. #1
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    Cool Patient w/ Diabetic Ketoacidosis

    Patient w/ Diabetic Ketoacidosis is vomiting. Both keto acidosis and vomiting are of equal severity. The arterial blood gas are most likely to exhibit which of the following changes in arterial pH, arterial carbon dioxide(PaCO2) and bicarbonate (HCO3)

    Increased= Inc
    Decreased= Dec
    Normal = Norm

    A. Norm pH, Norm PaCO2, norm HCO3
    B. Dec pH, Inc. PaCo2, Dec HCO3
    C. Inc. pH, Dec PaCo2, Inc. HCO3
    D. Norm pH, Inc. PaCo2, Inc HCO3
    E. Norm pH, Dec PaCO2, Dec HCO3

    I think its A?
    I procrastinate....

  2. #2
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    Thumbs up

    Vomiting may become very serious....I have seen a patient dying just after one episode of vomiting due to changes in electrolyte....This may help u for ur answer.......

    Respiratory Alkalosis

    Results from the excessive excretion of CO2, and occurs when the PaCO2 is less than 4.5kPa (34mmHg). This is commonly seen in hyperventilation due to anxiety states. In more serious disease states, such as severe asthma or moderate pulmonary embolism, respiratory alkalosis may occur. Here hypoxia, due to ventilation perfusion (V/Q) abnormalities, causes hyperventilation (in the spontaneously breathing patient). As V/Q abnormalities have little effect on the excretion of CO2 the patients tend to have a low arterial partial pressure of oxygen (PaO2) and low PaCO2.

    Metabolic Acidosis

    May result from either an excess of acid or reduced buffering capacity due to a low concentration of bicarbonate. Excess acid may occur due increased production of organic acids or, more rarely, ingestion of acidic compounds.

    a) Excess H+ Production: this is perhaps the commonest cause of metabolic acidosis and results from the excessive production of organic acids (usually lactic or pyruvic acid) as a result of anaerobic metabolism. This may result from local or global tissue hypoxia. Tissue hypoxia may occur in the following situations:
    Reduced arterial oxygen content: for example anaemia or reduced PaO2.
    Hypoperfusion: this may be local or global. Any cause of reduced cardiac output may result in metabolic acidosis (eg: hypovolaemia, cardiogenic shock etc). Similarly, local hypoperfusion in conditions such as ischaemic bowel or an ischaemic limb may cause acidosis.
    Reduced ability to use oxygen as a substrate. In conditions such as severe sepsis and cyanide poisoning anaerobic metabolism occurs as a result of mitochondrial dysfunction.

    Another form of metabolic acidosis is diabetic ketoacidosis. Cells are unable to use glucose to produce energy due to the lack of insulin. Fats form the major source of energy and result in the production of ketone bodies (aceto- acetate and 3-hydroxybutyrate) from acetyl coenzyme A. Hydrogen ions are released during the production of ketones resulting in the metabolic acidosis often observed.

    b) Ingestion of Acids: this is an uncommon cause of metabolic acidosis and is usually the result of poisoning with agents such as ethylene glycol (antifreeze) or ammonium chloride.

    c) Inadequate Excretion of +: this results from renal tubular dysfunction and usually occurs in conjunction with inadequate reabsorption of bicarbonate. Any form of renal failure may result in metabolic acidosis. There are also specific disorders of renal hydrogen ion excretion known as the renal tubular acidoses.

    Some endocrine disturbance may also result in inadequate H+ excretion e.g. hypoaldosteronism. Aldosterone regulates sodium reabsorption in the distal renal tubule. As sodium reabsorption and H+ excretion are linked, a lack of aldosterone (eg: Addison's disease) tends to result in reduced sodium reabsorption and, therefore, reduced ability to excrete H+ into the tubule resulting in reduced H+ loss. The potassium sparing diuretics may have a similar effect as they act as aldostrone antagonists.

    d) Excessive Loss of Bicarbonate: gastro- intestinal secretions are high in sodium bicarbonate. The loss of small bowel contents or excessive diarrhoea results in the loss of large amounts of bicarbonate resulting in metabolic acidosis. This may be seen in such conditions as Cholera or Crohn's disease.

    Acetazolamide, a carbonic anhydrase inhibitor, used in the treatment of acute mountain sickness and glaucoma, may cause excessive urinary bicarbonate losses. Inhibition of carbonic anhydrase slows the conversion of carbonic acid to CO2 and water in the renal tubule. Thus, more carbonic acid is lost in the urine and bicarbonate is not reabsorbed.

    Metabolic Alkalosis

    May result from the excessive loss of hydrogen ions, the excessive reabsorption of bicarbonate or the ingestion of alkalis.

    a) Excess H+ loss: gastric secretions contain large quantities of hydrogen ions. Loss of gastric secretions, therefore, results in a metabolic alkalosis. This occurs in prolonged vomiting for example, pyloric stenosis or anorexia nervosa.

    b) Excessive Reabsorption of Bicarbonate: as discussed earlier bicarbonate and chloride concentrations are linked. If chloride concentration falls or chloride losses are excessive then bicarbonate will be reabsorbed to maintain electrical neutrality. Chloride may be lost from the gastro-intestinal tract, therefore, in prolonged vomiting it is not only the loss of hydrogen ions that results in the alkalosis but also chloride losses resulting bicarbonate reabsorption. Chloride losses may also occur in the kidney usually as a result of diuretic drugs. The thiazide and loop diuretics a common cause of a metabolic alkalosis. These drugs cause increased loss of chloride in the urine resulting in excessive bicarbonate reabsorption.

    c) Ingestion of Alkalis: alkaline antacids when taken in excess may result in mild metabolic alkalosis. This is an uncommon cause of metabolic alkalosis.

    Compensation

    From earlier in the article it should be clear that the systems controlling acid base balance are interlinked. As explained earlier, maintenance of pH as near normal is vital, therefore dysfunction in one system will result in compensatory changes in the others. The three mechanisms for compensation mentioned earlier occur at different speeds and remain effective for different periods.
    Rapid chemical buffering: this occurs almost instantly but buffers are rapidly exhausted, requiring the elimination of hydrogen ions to remain effective.
    Respiratory compensation: the respiratory centre in the brainstem responds rapidly to changes in CSF pH. Thus, a change in plasma pH or PaCO2 results in a change in ventilation within minutes.
    Renal compensation: the kidneys respond to disturbances in acid base balance by altering the amount of bicarbonate reabsorbed and hydrogen ions excreted. However, it may take up to 2 days for bicarbonate concentration to reach a new equilibrium.

    These compensatory mechanisms are efficient and often return the plasma pH to near normal. However, it is uncommon for complete compensation to occur and over compensation does not occur.

    Interpretation of Acid Base Disturbances in Blood Gas Results

    Blood gas analysis is available in the vast majority of acute hospitals in the developed world. Increasingly blood gas machines are available for use in developing countries. In order to obtain meaningful results from any test it is important that they are interpreted in the light of the patient's condition. This requires knowledge of the patient's history and examination findings.

    The simplest blood gas machines measure the pH, PCO2 and PO2 of the sample. More complicated machines will also measure electrolytes and haemoglobin concentration. Most blood gas machines also give a reading for the base excess and/or standard bicarbonate. These values are used to assess the metabolic component of an acid base disturbance and are calculated from the measured values outlined above. They are of particular use when the cause of the acid base disturbance has both metabolic and respiratory components.
    The Base Excess: is defined as the amount of acid (in mmol) required to restore 1 litre of blood to its normal pH, at a PCO2 of 5.3kPa (40mmHg). During the calculation any change in pH due to the PCO2 of the sample is eliminated, therefore, the base excess reflects only the metabolic component of any disturbance of acid base balance. If there is a metabolic alkalosis then acid would have to be added to return the blood pH to normal, therefore, the base excess will be positive. However, if there is a metabolic acidosis, acid would need to be subtracted to return blood pH to normal, therefore, the base excess is negative.
    The Standard Bicarbonate: this is similar to the base excess. It is defined as the calculated bicarbonate concentration of the sample corrected to a PCO2 of 5.3kPa (40mmHg). Again abnormal values for the standard bicarbonate are only due the metabolic component of an acid base disturbance. A raised standard bicarbonate concentration indicates a metabolic alkalosis whilst a low value indicates a metabolic acidosis.

    The flow chart on the next page indicates how to approach the interpretation of acid base disturbances. First examine the pH; as discussed earlier a high pH indicates alkalaemia, whilst a low pH acidaemia. Next look at the PCO2 and decide whether it accounts for the change in pH. If the PCO2 does account for the pH then the disturbance is a primary respiratory acid base disturbance. Now look at the base excess or standard bicarbonate) to assess any metabolic component of the disturbance. Finally, one needs to decide if any compensation for the acid base disturbance has happened. Compensation has occurred if there is a change in the PCO2 or base excess in the opposite direction from that which would be expected from the pH. For example in respiratory compensation for a metabolic acidosis the PCO2 will be low. A low PCO2 alone causes an alkalaemia (high pH). The body is therefore using this mechanism to try to bring the low pH caused by the metabolic acidosis back towards normal.

    By now the complexity of acid base disturbance should be clear!! As in many complex concepts examples may clarify matters. In the following examples work through the flow charts to interpret the data.

    Example 1: A 70 year old man is admitted to the intensive car unit with acute pancreatitis. He is hypotensive, hypoxic and in acute renal failure. He has a respiratory rate of 50 breaths per minute. The following blood gas results are obtained:

    pH 7.1

    PCO2 3.0kPa (22mmHg)

    BE -21.0mmol

    From the flow charts: firstly, he has a severe acidaemia (pH 7.1). The PCO2 is low, which does not account for the change in pH (a PCO2 of 3.0 would tend to cause alkalaemia). Therefore, this cannot be a primary respiratory acidosis. The base excess of -21 confirms the diagnosis of a severe metabolic acidosis. The low PCO2 indicates that there is a degree of respiratory compensation due to hyperventilation. These results were to be expected given the history.

    Example 2: A 6 week old male child is admitted with a few days history of projectile vomiting. The following blood gases are obtained:

    pH 7.50

    PCO2 6.5kPa (48mmHg)

    BE +11.0mmol


    The history points to pyloric stenosis. There is an alkalaemia, which is not explained by the PCO2. The positive base excess confirms the metabolic alkalosis. The raised PCO2 indicates that there is some respiratory compensation.


    For more u can refer to:
    [HIDE]
    http://www.health.adelaide.edu.au/pa.../AcidBase.html[/HIDE]

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