Clearly I was concerned that this patient would be very sick and may not tolerate general anesthetic. A quick review of his other medications revealed that he was not requiring any vasopressors. This came to me as surprise. My first guess as to the etiology of this man's severe acidemia was septic induced lactic acidosis. I guessed that he was coming to the OR by urology due to a stone obstructing the ureters resulting in urosepsis that had lead to hypovolemia and a profound vasodilated state that had caused hypoperfusion of his organs and lead to a severe metabolic acidosis resulting from lactate. However, upon meeting the patient, it seemed that this cause was not likely as he had no problems with his blood pressure which indeed was slightly elevated. A quick exam revealed an elderly bearded and disheveled gentleman who was essentially comatose with obvious and exaggerated kussmaul respirations.
I accompanied the patient to the OR, and decided given his near comatose state to use no anesthetics until proven necessary as I was still unsure as to the etiology of his severely compromised state. The urologist performed cystoscopy with a rigid scope first. This resulted in movement and groaning from the patient. I administered 25 mcg of fentanyl and adminstered 1% sevoflurane in oxygen via a mask strapped to his face. The acutal ET Sevo concentration reached about 0.9% and this plus 25 mcg fentanyl allowed the case to continue which included placement of a suprapubic catheter to empty the bladder. The patient was found to have a false lumen in his urethra which had complicated a previous attempt at placement of a foley catheter. The patient tolerated the anesthesia well with blood pressures staying relatively elevated and saturations remaining near 100%. The patient continued vigorous ventilation throughout and I made no attempt to suppress this.
Acid base disorders are frequently encountered by anesthesiologists in the OR. A rapid decision tree is required by anesthesiologists to deal with these disorders as we often have little time to tinker with long complicated differential diagnoses and mathematical calculations. Therefore a rapid stepwise approach is necessary to distill the important clinical aspects that will impact upon anesthetic care while ignoring aspects of the syndrome that have no bearing on our approach to the patient.
Acidosis is of concern to the anesthesiologist as it causes impaired cardiac contractility, can decrease the threshold for V fib, may decrease hepatic and renal blood flow, can increase pulmonary vascular resistance and reduces the responsiveness of the adrenergic receptors to catecholamines. Furthermore, acidosis can inhibit coagulation factors and platelets and may result in vascular collapse. Of course, the etiology of the acidosis is likely more impactful than the actual degree of acidosis. Therefore, determining the underlying cause of the patient's acidosis may be more important than knowing the exact pH.
Acidosis is of concern to the anesthesiologist as it causes impaired cardiac contractility, can decrease the threshold for V fib, may decrease hepatic and renal blood flow, can increase pulmonary vascular resistance and reduces the responsiveness of the adrenergic receptors to catecholamines. Furthermore, acidosis can inhibit coagulation factors and platelets and may result in vascular collapse. Of course, the etiology of the acidosis is likely more impactful than the actual degree of acidosis. Therefore, determining the underlying cause of the patient's acidosis may be more important than knowing the exact pH.
There are three main approaches to acid base disorders. 1) The traditional approach learned by most medical students, 2) the base excess (BE) approach, and 3) the physio chemical approach (Stewart approach). The traditional approach in conjunction with the BE method is most practical especially for clinicians in a rapidly changing environments. The Stewart approach is best for analyzing more complex or arcane acid base disorders that require a high degree of accuracy for treatment. One important point to keep in mind when using the traditional method of Acid Base analysis is to correct for hypoalbuminemia when significant. This is because Albumin provides a large negative buffer in the serum and when low, can have a profound effect on the anion gap. For simplicity, online calculators are available to quickly determine the corrected anion gap. I also recomment the free app "ABG interpreter" in the android market place. Rather then trying to remember the equation (Corrected AGAP=Observed AGAP +2.5 x (4.5-measured Albumin) it is preferable to understand that the correction is required and where to quickly make this calculation.
In the traditional approach, a quick determination of the primary disorder is based on the pH (acidemic or alkalemic) based on an arterial blood sample. Next, a determination of whether the primary disorder is metabolic or respiratory is made by looking at the CO2. If the patient is found to have a primary metabolic acidosis, then you must determine whether it is a non gap or gap acidosis. My patient had an anion gap of >30. Calculating the anion gap is always important regardless of the measured pH since an anion gap of greater than 20 indicates a primary metabolic acidosis regardless of measured pH. The MUDPILES acronym often helps us remember the causes of the GAP acidoses (methanol, uremia, DKA, paraldehyde,INH or infection, lactic, Ethylene glycol, or Salicylates). However, this acronym is not all inclusive; you must remember to include starvation and alcohol induced ketosis, Toluene (if early) and propylene glycol. This last one may be seen in patients who have been in the ICU receiving non water soluble medications such as lorazepam. Respiratory compensation is expected with metabolic acidosis and this is referred to as Kussmaul respirations. Acidosis stimulates receptors in the medulla to increase the minute ventilation, mitigating the decrease in pH, but this compensation is never complete. The expected degree of compensation can be calculated using the winter equation (preferable to use the free app to save time). A quick calculation using Winter's formula in my patient revealed estimated Pco2 = 1.5 x HCO3 +8= 1.5 x 9 +8= 21.5 mm Hg. My patient's PCO2 was actually 7.1 mmHg. Since this is considerably lower than what is expected, it can be said that this patient had a primary metabolic acidosis with secondary respiratory alkalosis (i.e. his minute ventilation was greater than anticipated for his degree of acidemia). Since this patient had a large anion gap it was necessary to verify that the bicarbonate concentration had decreased enough to account for the increase in anion gap. In other words, if you simply assume that you have a anion gap metabolic acidosis, and don't precisely measure the expected change in bicarbonate vs. increase in anion gap, you may miss a concomitant non gap metabolic acidosis (i.e. from a patient with a lactic acidosis who had been vomiting). This is accomplished by calculating the delta gap/delta bicarb ratio. In my patient the anion gap is (144-(101+9)=34 and a normal anion gap is 10 to 12, so the difference is 34-12=22. This means I should see the patients HCO3- decrease by about 22 mEq/L. The normal HCO3- is 24 mEq/L and the patients HCO3- is 9, so 24-9=15. The ratio is calculated by taking the difference of the change in anion gap from normal divided by the change in bicarbonate or 22/15=1.5. This is known as the "gap-gap" or the "delta-delta". The formula is delta-delta = (mAG-12)/(24-mHCO3-). This is important because if your ratio is less than 1, it indicates that the decrease in HCO3- is greater than the increase in the AGAP. This would indicate that there is another source for the acidosis. In that case you would say that you have a patient with a primary anion gap metabolic acidosis with a co existing non gap acidosis. However, if alkali is added to the patient, then the delta-delta ratio will be greater than 1. This indicates there is a co existent metabolic alkalosis. In our case, the ratio is 1.6 and thus, there is a co existent metabolic alkalosis. In this patient this most likely resulted from treatment with bicarbonate infusion.
In this case the cause of the patients significant respiratory alkalosis is puzzling. The lab tests on this patient indicated that he had not ingested aspirin, a possible cause of a combined metabolic acidosis with respiratory alkalosis. Other causes of respiratory alkalosis include: hypoxemic drive, pulmonary disease with A-a gradient, cardiac disease with a right to left shunt, pulmonary edema, high altitude, emphysema, PE, CNS disease with stimulation of the respiratory center, pain, psychogenic, liver failure with encephalopathy, sepsis/infection, salicylates, progesterone, pregnancy, and severe fever. This patient did not have any obvious source for his severe respiratory alkalosis. The severe hyperventilation (PaCO2 of 9 mm Hg) was concerning to me in that severe hypocapnea causes cerebral vasoconstriction and seemingly could induce ischemic brain injury due to decreased CBF. Severe alkalosis is also associated with a lowered seizure threshold and seizure activity. In fact, as an aside, this patient did have a seizure early the next morning before dialysis was begun. In particular, several studies that have brought PCO2 tensions down to below 16 mm Hg in humans and animals have demonstrated a decrease in CMRO2 in the brain which indicates insufficient cerebral blood flow. However, to the degree that cerebral ischemia occurs, local Hydrogen and potassium levels increase and may cause a rebound vasodilation. This results in regional areas of increased blood flow mixed with areas of intense vasoconstriction. Evidence suggests that this decrease in CBF will continue for a number of hours after the onset of hyperventilation, but with time, CSF pH will drop globally, and CBF will creep back up towards normal (most estimate after 6 to 8 hours of hyperventilation). In any case, This man's significant respiratory alkalosis was potentially detrimental. At this point, the anesthesiologist needs to consider two possible choices: 1) provide significant narcotic sedation leading to decreased minute ventilation and improving the respiratory alkalosis which would improve cerebral vasoconstriction, or 2) minimize narcotic sedation to avoid acutely decreasing minute ventilation so as not to cause a rebound increase in ICP. This second consideration is important if the patient has been hyperventilating for longer than 8 to 10 hours. I opted to maintain the patient's status quo given that I still did not have all of the information and it wasn't clear to me exactly how long this patient had been hyperventilating given that his first blood gas obtained already demonstrated a significant respiratory alkalosis. However, the ventilation management of this patient does not only depend upon the respiratory portion of his acid base status.
Patients with a significant metabolic acidosis requiring intubation are at risk for subsequent destabilization if elevated minute ventilation is not provided. In these cases, the respiratory compensation is lost when the vent settings are inappropriate, the PCO2 drifts back up toward the normal range of 40 mm Hg resulting in a dramatic increase in acidemia. This significant acid load can cause cardiac failure with vasoplegia resulting in an abrupt circulatory decompensation Therefore, after instituting mechanical ventilation in a acidemic patient, it is prudent to use winter's formula to estimate the aproximate PCO2 level that would be expected to compensate for the degree of acidosis. This patient had a primary metabolic acidosis due to his AGAP greater than 20 mEq/L. To determine the etiology or source of the unmeasured anion clinical history and exam plus laboratory measurements are required. The most frequent cause of AGAP acidosis is type A lactic acidosis due to hypoperfusion of organs. Our patient most likely did have some degree of lactic acidosis as he appeared to be hypovolemic as measured by his elevated Hgb of 17.5 g/dL. However, his lactate was measured at 2.5 mmol/L. Usually a lactate of greater than 4 mmol/L is associated with significantly worse outcome and can be an early sign of occult severe sepsis.
In this case the cause of the patients significant respiratory alkalosis is puzzling. The lab tests on this patient indicated that he had not ingested aspirin, a possible cause of a combined metabolic acidosis with respiratory alkalosis. Other causes of respiratory alkalosis include: hypoxemic drive, pulmonary disease with A-a gradient, cardiac disease with a right to left shunt, pulmonary edema, high altitude, emphysema, PE, CNS disease with stimulation of the respiratory center, pain, psychogenic, liver failure with encephalopathy, sepsis/infection, salicylates, progesterone, pregnancy, and severe fever. This patient did not have any obvious source for his severe respiratory alkalosis. The severe hyperventilation (PaCO2 of 9 mm Hg) was concerning to me in that severe hypocapnea causes cerebral vasoconstriction and seemingly could induce ischemic brain injury due to decreased CBF. Severe alkalosis is also associated with a lowered seizure threshold and seizure activity. In fact, as an aside, this patient did have a seizure early the next morning before dialysis was begun. In particular, several studies that have brought PCO2 tensions down to below 16 mm Hg in humans and animals have demonstrated a decrease in CMRO2 in the brain which indicates insufficient cerebral blood flow. However, to the degree that cerebral ischemia occurs, local Hydrogen and potassium levels increase and may cause a rebound vasodilation. This results in regional areas of increased blood flow mixed with areas of intense vasoconstriction. Evidence suggests that this decrease in CBF will continue for a number of hours after the onset of hyperventilation, but with time, CSF pH will drop globally, and CBF will creep back up towards normal (most estimate after 6 to 8 hours of hyperventilation). In any case, This man's significant respiratory alkalosis was potentially detrimental. At this point, the anesthesiologist needs to consider two possible choices: 1) provide significant narcotic sedation leading to decreased minute ventilation and improving the respiratory alkalosis which would improve cerebral vasoconstriction, or 2) minimize narcotic sedation to avoid acutely decreasing minute ventilation so as not to cause a rebound increase in ICP. This second consideration is important if the patient has been hyperventilating for longer than 8 to 10 hours. I opted to maintain the patient's status quo given that I still did not have all of the information and it wasn't clear to me exactly how long this patient had been hyperventilating given that his first blood gas obtained already demonstrated a significant respiratory alkalosis. However, the ventilation management of this patient does not only depend upon the respiratory portion of his acid base status.
Patients with a significant metabolic acidosis requiring intubation are at risk for subsequent destabilization if elevated minute ventilation is not provided. In these cases, the respiratory compensation is lost when the vent settings are inappropriate, the PCO2 drifts back up toward the normal range of 40 mm Hg resulting in a dramatic increase in acidemia. This significant acid load can cause cardiac failure with vasoplegia resulting in an abrupt circulatory decompensation Therefore, after instituting mechanical ventilation in a acidemic patient, it is prudent to use winter's formula to estimate the aproximate PCO2 level that would be expected to compensate for the degree of acidosis. This patient had a primary metabolic acidosis due to his AGAP greater than 20 mEq/L. To determine the etiology or source of the unmeasured anion clinical history and exam plus laboratory measurements are required. The most frequent cause of AGAP acidosis is type A lactic acidosis due to hypoperfusion of organs. Our patient most likely did have some degree of lactic acidosis as he appeared to be hypovolemic as measured by his elevated Hgb of 17.5 g/dL. However, his lactate was measured at 2.5 mmol/L. Usually a lactate of greater than 4 mmol/L is associated with significantly worse outcome and can be an early sign of occult severe sepsis.
As the lactate was low and ketones were negative in the urine another source for his anion gap is likely. The serum osmolality can often provide a clue as to the cause of a gap metabolic acidosis. Ingested intoxicants can increase the serum osmolality. If the Laboratory value is greater than the calculated value by more than ten it is good evidence that your GAP metabolic acidosis is a result of an ingested intoxicant. (i.e. calOSM-measOSM <10 p="p">
Ethylene glycol (antifreeze) is metabolized in the liver to glycolic acid which accounts for the metabolic acidosis. Further metabolism to oxalic acid can cause ca2+ oxalate crystals to be deposited into the tissues and spill into the urine where they are visible upon microscopic examination. These crystals can also cause hypocalcemia, renal failure, cardiopulmonary dysfunction, and neurologic dysfunction. In fact, the calcium oxalate crystals may be the only clue to diagnosis if found late as the ethylene glycol is metabolized and may be negative on tox screen. After ingestion of a significant amount of ethylene glycol, the patient will encounter three phases of morbidity. Stage 1, the acute phase, results in acute CNS depression mimicking acute alcohol intoxication. Hyperosmolarity is also encountered during this phase. These effects last from 30 min to 12 hours after ingestion and recede as the last of the ethylene glycol is metabolized. Phase two lasts from 12 to 24 hours after ingestion and is caused by the metabolites of the ethylene glycol. These result in the severe metabolic acidosis with respiratory compensation, and the hyperosmolar state begins to recede as the ethylene glycol is metabolized. During this time period calcium oxalate crystals are deposited into the brain, heart, kidneys, and lungs and result in damage to these structures based on the degree of deposition. Phase three lasts from 24 hours to 72 hours from the direct toxic affects of the metabolites on the major organs. In most cases the kidneys are the organ most effected causing complete renal failure. Oxalic, glyoxylic, glycolic acid metabolites in addition to the calcium oxalate crystals are directly cytotoxic to the tubular cells in the kidney leading to acute tubular necrosis.
This patient needed to receive volume replacement and NaHCO3- to promote urinary excretion of the ethylene glycol. However, ethylene glycol is toxic to kidneys and indeed this patient suffered AKI and required hemodialysis. HD is indeed very effective in treating ethylene glycol intoxication and reducing the acidosis. Fomepizole is another treatment for ethylene glycol intoxication. Fomepizole inhibits alcohol dehydrogenase the enzyme responsible for the metabolism of ethylene glycol, ethanol, and methanol.
While sodium bicarbonate is recommended in this type of metabolic acidosis, in many cases it is not helpful. However, when the pH is less than 7.0, cardiac contractility is significantly inhibited and sodium bicarb may be helpful. Whether to give sodium bicarb depends largely on the etiology of the acidosis and whether the patient can tolerate and would benefit from a sodium load. It is clearly beneficial in patients who have a relative Na deficiency compared to chloride ion (i.e. hyperchloremic non gap acidosis) or when it is evident that the patient is spilling bicarbonate into the urine or from losses into the large intestine. However, in treating metabolic acidosis where the non measured anions will be converted readily back into bicarbonate (read ketoacids, lacatate) giving bicarbonate may not be helpful and could even be harmful as the CO2 generated may enter the cell and worsen intracellular acidosis. This is most common in low flow states after cardiac arrest. In this case, ethylene glycol is metabolized into acid that will not be converted into bicarbonate and alkalinizing the urine can be helpful in excreting ethylene glycol. The dose to give is calculated based on the extracellular space which is 25% of body weight. However, it is assumed that some amount of bicarbonate will find its way into the cells, and therefore, increasing the bicarbonate space up to 30% of the body weight is common. To determine how much bicarbonate will be needed is is important to determine the base deficit which is usually provided when an ABG is sent to the lab. For example, my patient had a BD of 25 mEq/L. Therefore, BD X bicarb space X body weight (in Liters)= Bicarb dose and would be 25 mEq/L X .3 X 80 L= 600 mEq. Usually, one half of the dose is given and another blood gas is drawn to recalibrate.
The procedure was quick and the patient was returned to the ICU at his baseline: high minute ventilation with significant acidosis, but HD stable. That night HD was begun with a bicarbonate dialysate. His metabolic acidosis resolved, minute ventilation returned to normal, and he was A&O x 3.
While sodium bicarbonate is recommended in this type of metabolic acidosis, in many cases it is not helpful. However, when the pH is less than 7.0, cardiac contractility is significantly inhibited and sodium bicarb may be helpful. Whether to give sodium bicarb depends largely on the etiology of the acidosis and whether the patient can tolerate and would benefit from a sodium load. It is clearly beneficial in patients who have a relative Na deficiency compared to chloride ion (i.e. hyperchloremic non gap acidosis) or when it is evident that the patient is spilling bicarbonate into the urine or from losses into the large intestine. However, in treating metabolic acidosis where the non measured anions will be converted readily back into bicarbonate (read ketoacids, lacatate) giving bicarbonate may not be helpful and could even be harmful as the CO2 generated may enter the cell and worsen intracellular acidosis. This is most common in low flow states after cardiac arrest. In this case, ethylene glycol is metabolized into acid that will not be converted into bicarbonate and alkalinizing the urine can be helpful in excreting ethylene glycol. The dose to give is calculated based on the extracellular space which is 25% of body weight. However, it is assumed that some amount of bicarbonate will find its way into the cells, and therefore, increasing the bicarbonate space up to 30% of the body weight is common. To determine how much bicarbonate will be needed is is important to determine the base deficit which is usually provided when an ABG is sent to the lab. For example, my patient had a BD of 25 mEq/L. Therefore, BD X bicarb space X body weight (in Liters)= Bicarb dose and would be 25 mEq/L X .3 X 80 L= 600 mEq. Usually, one half of the dose is given and another blood gas is drawn to recalibrate.
The procedure was quick and the patient was returned to the ICU at his baseline: high minute ventilation with significant acidosis, but HD stable. That night HD was begun with a bicarbonate dialysate. His metabolic acidosis resolved, minute ventilation returned to normal, and he was A&O x 3.
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