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Abg intepretation case scenario


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this real case scenario dicussing ABG interpritation

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Abg intepretation case scenario

  1. 1. ABG interpretation case scenario Kamal Osman Mergani Consultant intensivist
  2. 2. Case presentation <ul><li>‎ 15 Y/O male patient underwent craniotomy and resection of a fronto-temporal tumor. </li></ul><ul><li>After around 5 hours uneventful surgery, he was extubated and transferred to ICU. He was conscious with GA residual effects, hemodynamically stable, spontaneously breathing on O2 8 LPM via face mask with good urine output </li></ul>
  3. 3. ABG <ul><li>Initial ABG showed the following results: pH: 7.22 pCO2: 36.7 pO2: 181.5 HCO3-: 14.7 SaO2: 99.6% </li></ul>
  4. 4. ABG <ul><li>Na: 141 K: 3.9 Cl: 104 Ca++: 1.15 Hb: 127 Lactate: 7.8 </li></ul>
  5. 5. <ul><li>What is your impression and management ?? </li></ul>
  6. 6. ABG analalysis <ul><ul><li>pH of 7.22 and HCO3 of 14.7 indicating metabolic academia. Predicted PCO2 (Respiratory compensation): PCO2= 1.5 X[HCO3]+8 </li></ul></ul><ul><ul><li>therefore PCO2 should have been </li></ul></ul><ul><ul><li>1.5X14.7+8= 30 </li></ul></ul><ul><ul><li>but actual is 36.7 indicating combined respiratory and metabolic acidosis </li></ul></ul>
  7. 7. ABG analalysis <ul><li>AG= Na-(Cl+HCO3)= 141-(104+15)= 22 ∆ AG= 22-12= 10 ∆ HCO3= 24-15= 9 Thus ∆ HCO3 = ∆ AG indicating no combined non-anion gap metabolic acidosis </li></ul><ul><li>Added anions= 10 mmol/L= 8 Lactic acid + 2 ? </li></ul>
  8. 8. ABG analalysis <ul><li>Final diagnosis combined metabolic lactic acidosis indicating hypoperfusion and respiratory acidosis indicating respiratory suppression secondary to residual general anesthesia effects. </li></ul>
  9. 9. <ul><li>HR was around 100↑ and CVP around 5↓ </li></ul>
  10. 10. F/U of patient <ul><li>As the patient is more awake now and with the resolution of general anesthesia effects, it is clear that the patient now has metabolic acidosis with full respiratory compensation secondary to lactic acidosis </li></ul>
  11. 11. Lactic acidosis <ul><li>The most frequent cause of lactic acidosis is type A that is secondary to poor tissue perfusion, which is induced by various shock states causing tissue hypoxia, but you are ruling out any hypotension in the peri-operative period! </li></ul>
  12. 12. <ul><li>Type B1 , has been identified with diabetes mellitus, bowel ischemia, severe iron-deficiency anemia, liver disease, alcoholic ketoacidosis, pancreatitis, malignancy (leukemia, lymphoma, lung cancer), infection, renal failure, seizures, heat stroke, pheochromocytoma, thiamine deficiency, short gut syndrome, and other carbohydrate malabsorption syndromes </li></ul>
  13. 13. Type B2 lactic acidosis <ul><li>Medicinal and toxic causes of lactic acidosis, known as type B2 , are numerous, including acetaminophen, alcohols and glycols (ethanol, ethylene glycol, methanol, propylene glycol), antiretroviral nucleoside analogs (zidovudine, didanosine, ...lamivudine), </li></ul>
  14. 14. Type B2 lactic acidosis <ul><ul><li>Beta-adrenergic agents (epinephrine, ritodrine, terbutaline), biguanides (phenformin, metformin), cocaine, cyanogenic compounds (cyanide, aliphatic nitriles, nitroprusside), diethyl ether, 5-fluorouracil, halothane, iron, isoniazid, propofol, sugars and sugar alcohols (fructose, sorbitol, and xylitol), salicylates, strychnine, sulfasalazine, and valproic acid. </li></ul></ul>
  15. 15. Type B3 lactic acidosis <ul><li>B3 lactic acidosis may result in those with inborn errors of metabolism. These include glucose-6-phosphatase deficiency (von Gierke disease), fructose-1,6-diphosphatase deficiency, pyruvate carboxylase deficiency, pyruvate dehydrogenase deficiency, oxidative phosphorylation deficiency, and methylmalonic aciduria </li></ul>
  16. 16. <ul><li>Lactic acidosis rarely may present in the MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and stroke like episodes), which appears to be caused by a point mutation in mitochondrial DNA tRNALeu (UUR) gene. This syndrome is characterized by migraine like headaches, dementia, hearing loss, ataxia, and episodic vomiting. </li></ul>
  17. 17. Back to the patient <ul><li>Patient was managed with NS boluses of total 1.5 L since the admission to ICU. </li></ul><ul><li>The lactate level dropped to 4.3 after 4 hours of the last ABG then to 0.8 after 12 hours of ICU admission. </li></ul><ul><li>This will rule out type B1 and the toxic (medical) causes </li></ul>
  18. 18. <ul><li>The explanation was possible hypothermia during the anesthesia which is common in the neurosurgical procedures (and may be severe shivering during the recovery). The lactate level will start to increase during the warming periods and continues for hours before starting clearance. Probably there is some metabolic disorder as well made it so severe. </li></ul>