基本上. 我的建議是能不給就不給. 如果你堅持要給. 請說明你的理由.
醫療決策不該只治療數據. 給予碳酸氫鈉將目前 pH 值暫時校正回來.
可能會誤判 DKA 已經控制
事實上. 血液氣體分析的 pH 值, 是決定是否繼續施打靜脈胰島素的重要指標
DKA 缺的是胰島素. 當然也會合併一些脫水( NKHS 非酮酸中毒之高滲透壓血症. 脫水問題會比DKA 更嚴重)
急診醫師教科書 ROSEN (忘了當初是看第幾版了) 關於 DKA部分. page 1634
裡面說. sodium bicarbonate 不建議泡在 normal saline 內使用. 因為滲透壓太高
pH < 7.1 每公斤給 1mEq. 一支NaHCO3 約 17 mEq. 成人一次可以補 3-4 支
不建議例行補充. 很多醫師甚至 pH 6.7 以上都建議不要給.
治療目標. 將 pH 校正到 7.1 即可. 讓 HCO3 上升 10 mEq/L
使用方式. 將 NaHCO3 泡在 D5W 裡面. 九支泡一公升.
考慮到這些潛在危害且缺乏已證實的益處，許多作者質疑即使在嚴重酸血症的情況下碳酸氫鹽治療的效用。 13 然而，儘管缺乏證據，但通常建議根據經驗使用碳酸氫鈉治療血清pH值低於7.1。 1 mEq/kg，除非潛在的酸中毒被認為對治療有快速反應。14 然而，許多專家不會治療pH 值高於6.7 的情況，尤其是糖尿病酮症酸中毒，在糾正潛在病變的同時，通常可以很好地耐受嚴重酸血症。治療終點包括 pH 值高於 7.1 和血清碳酸氫鹽濃度高於 10 mEq/L。通過添加 150 mEq 碳酸氫鈉（三個“急救車安瓿”，通常為 50 mL，每瓶 8 個）來製備碳酸氫鹽滴注。4% 溶液）加入 1 升 5% 葡萄糖水溶液中，並在臨床情況允許的情況下緩慢輸注。出於高滲的考慮，碳酸氫鈉通常不應添加到生理鹽水中。
Many authors question the utility of bicarbonate therapy even in cases of severe acidemia, given these potential harms and the absence of demonstrated benefit.13 However, although evidence is lacking, it is commonly recommended to treat serum pH less than 7.1 empirically with sodium bicarbonate, 1 mEq/kg, unless the underlying acidosis is thought to be quickly responsive to therapy.14 Many experts will not treat pH above 6.7, however, especially in diabetic ketoacidosis, in which profound acidemia is usually well tolerated while the underlying lesion is corrected. Endpoints of therapy include pH above 7.1 and serum bicarbonate concentration above 10 mEq/L. A bicarbonate drip is prepared by adding 150 mEq sodium bicarbonate (three “crash cart ampules,” which are usually 50 mL of 8.4% solution) to 1 liter of 5% dextrose in water and infusing as slowly as the clinical situation permits. Sodium bicarbonate should generally not be added to normal saline for concern of hypertonicity.
下面資料來自 uptodate
Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment
碳酸氫鹽和代謝性酸中毒 — 如果動脈 pH 值低於 6.90，我們建議使用碳酸氫鹽。如果血清鉀低於 5.3 mEq/L，我們會在 400 mL 無菌水中加入 100 mEq 碳酸氫鈉和 20 mEq氯化鉀，給藥時間超過 2 小時。
Bicarbonate and metabolic acidosis — We suggest administering bicarbonate if the arterial pH is less than 6.90. We give 100 mEq of sodium bicarbonate in 400 mL sterile water with 20 mEq of potassium chloride, if the serum potassium is less than 5.3 mEq/L, administered over two hours.
應每兩小時監測一次靜脈 pH 值和碳酸氫鹽濃度，並且可以重複碳酸氫鹽劑量，直到 pH 值升至 7.00 以上（參見下面的“監測”）。當碳酸氫鹽 (HCO3) 濃度增加時，血清 K 值可能會下降，可能需要更積極的 KCl 補充。
The venous pH and bicarbonate concentration should be monitored every two hours, and bicarbonate doses can be repeated until the pH rises above 7.00 (see 'Monitoring' below). When the bicarbonate (HCO3) concentration increases, the serum K may fall and more aggressive KCl replacement may be required.
DKA 中碳酸氫鹽治療的適應症存在爭議[ 34 ]，並且缺乏益處的證據[ 35-37 ]。在一項對 21 名入院動脈 pH 值在 6.90 至 7.14（平均 7.01）之間的 DKA 患者進行的隨機試驗中，碳酸氫鹽治療並未改變發病率或死亡率[ 35 ]。然而，該研究規模較小，僅限於動脈pH值6.90及以上的患者，碳酸氫鹽組和安慰劑組之間動脈pH值和血清碳酸氫鹽的上升率沒有差異。尚未進行有關在 pH 值低於 6.90 的 DKA 中使用碳酸氫鹽的前瞻性隨機試驗。
The indications for bicarbonate therapy in DKA are controversial [34], and evidence of benefit is lacking [35-37]. In a randomized trial of 21 DKA patients with an admission arterial pH between 6.90 and 7.14 (mean 7.01), bicarbonate therapy did not change morbidity or mortality [35]. However, the study was small, limited to patients with an arterial pH 6.90 and above, and there was no difference in the rate of rise in the arterial pH and serum bicarbonate between the bicarbonate and placebo groups. No prospective randomized trials have been performed concerning the use of bicarbonate in DKA with pH values less than 6.90.
碳酸氫鹽的給藥也存在爭議，因為除了缺乏證據證明其益處外，還存在一些潛在的有害影響： ●如果碳酸氫鹽輸注成功地增加了血液碳酸氫鹽濃度，則可以
Bicarbonate administration is also controversial because in addition to lack of evidence for benefit, there are several potential harmful effects:
減少過度換氣驅動，從而升高血液pCO2。血液 CO2 張力的增加比動脈 HCO3 的增加更快地反映在血腦屏障上。這可能會導致大腦 pH 值的反常下降。儘管神經系統惡化已歸因於這種機制，但它仍然是一個非常有爭議的效應，而且即使發生，也很少見[ 38 ]。
●If bicarbonate infusion successfully increases the blood bicarbonate concentration, this can reduce the hyperventilatory drive, which will raise the blood pCO2. Increased blood CO2 tension is more quickly reflected across the blood brain barrier than the increased arterial HCO3. This may cause a paradoxical fall in cerebral pH. Although neurologic deterioration has been attributed to this mechanism, it remains a very controversial effect and, if it occurs, is rare [38].
●服用鹼可能會減慢酮症的恢復速度[ 39,40]。在一項針對七名患者的研究中，三名接受碳酸氫鹽治療的患者血清酮酸陰離子水平升高，酮症消退延遲六小時[39 ]。動物研究表明，碳酸氫鹽輸注可以加速生酮。這被認為與酸血症對有機性酸中毒有“制動作用”有關。任何增加全身 pH 值的操作都會減弱這種制動作用 [ 35 ]。
●The administration of alkali may slow the rate of recovery of the ketosis [39,40]. In a study of seven patients, the three patients treated with bicarbonate had a rise in serum ketoacid anion levels and a six-hour delay in resolution of ketosis [39]. Animal studies indicate that bicarbonate infusion can accelerate ketogenesis. This is thought to be related to the fact that acidemia has a “braking effect” on organic acidosis. This brake is lessened by any maneuver that increases systemic pH [35].
●給予鹼可導致治療後代謝性鹼中毒，因為酮酸陰離子與胰島素的代謝會導致碳酸氫根的產生，並自發糾正大部分代謝性酸中毒。(參見“成人糖尿病酮症酸中毒和高滲性高血糖狀態：流行病學和發病機制”，關於‘陰離子間隙代謝性酸中毒’一節)
●Alkali administration can lead to a posttreatment metabolic alkalosis, since metabolism of ketoacid anions with insulin results in the generation of bicarbonate and spontaneous correction of most of the metabolic acidosis. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis", section on 'Anion gap metabolic acidosis'.)
There are, however, selected patients who may benefit from cautious alkali therapy [38]. They include:
●Patients with an arterial pH ≤6.9 in whom decreased cardiac contractility and vasodilatation can further impair tissue perfusion [41,42]. At an arterial pH above 7.00, most experts agree that bicarbonate therapy is not necessary, since therapy with insulin and volume expansion largely reverse the metabolic acidosis [43].
●Patients with potentially life-threatening hyperkalemia, since bicarbonate administration in acidemic patients may drive potassium into cells, thereby lowering the serum potassium concentration [44]. (See"Treatment and prevention of hyperkalemia in adults".)
一篇 2011 年回顧文章說. 沒有證據顯示在 DKA 給予 bicarbonate 有好處. 尤其是兒科病人. 在 pH 6.9 以下也缺乏足夠證據給予建議.
處理目標, 減少高氯酸中毒, 減少 CSF 酸化, 減少腦水腫.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224469/
Conclusions
The evidence to date does not support the use of bicarbonate administration for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical and physiological harm and the lack of clinical or sustained physiological benefits. There also is insufficient evidence to justify the recommendation of bicarbonate administration in more extreme acidemia of pH < 6.90. Future research should focus on the use of more balanced and physiological resuscitation fluids with buffering capacity, in the modern context of DKA management, with the goal of reducing the component of hyperchloremic acidosis in DKA while minimizing the risk of CSF acidosis and associated CE
裡面說. sodium bicarbonate 不建議泡在 normal saline 內使用. 因為滲透壓太高
pH < 7.1 每公斤給 1mEq. 一支NaHCO3 約 17 mEq. 成人一次可以補 3-4 支
不建議例行補充. 很多醫師甚至 pH 6.7 以上都建議不要給.
治療目標. 將 pH 校正到 7.1 即可. 讓 HCO3 上升 10 mEq/L
使用方式. 將 NaHCO3 泡在 D5W 裡面. 九支泡一公升.
考慮到這些潛在危害且缺乏已證實的益處，許多作者質疑即使在嚴重酸血症的情況下碳酸氫鹽治療的效用。 13 然而，儘管缺乏證據，但通常建議根據經驗使用碳酸氫鈉治療血清pH值低於7.1。 1 mEq/kg，除非潛在的酸中毒被認為對治療有快速反應。14 然而，許多專家不會治療pH 值高於6.7 的情況，尤其是糖尿病酮症酸中毒，在糾正潛在病變的同時，通常可以很好地耐受嚴重酸血症。治療終點包括 pH 值高於 7.1 和血清碳酸氫鹽濃度高於 10 mEq/L。通過添加 150 mEq 碳酸氫鈉（三個“急救車安瓿”，通常為 50 mL，每瓶 8 個）來製備碳酸氫鹽滴注。4% 溶液）加入 1 升 5% 葡萄糖水溶液中，並在臨床情況允許的情況下緩慢輸注。出於高滲的考慮，碳酸氫鈉通常不應添加到生理鹽水中。
Many authors question the utility of bicarbonate therapy even in cases of severe acidemia, given these potential harms and the absence of demonstrated benefit.13 However, although evidence is lacking, it is commonly recommended to treat serum pH less than 7.1 empirically with sodium bicarbonate, 1 mEq/kg, unless the underlying acidosis is thought to be quickly responsive to therapy.14 Many experts will not treat pH above 6.7, however, especially in diabetic ketoacidosis, in which profound acidemia is usually well tolerated while the underlying lesion is corrected. Endpoints of therapy include pH above 7.1 and serum bicarbonate concentration above 10 mEq/L. A bicarbonate drip is prepared by adding 150 mEq sodium bicarbonate (three “crash cart ampules,” which are usually 50 mL of 8.4% solution) to 1 liter of 5% dextrose in water and infusing as slowly as the clinical situation permits. Sodium bicarbonate should generally not be added to normal saline for concern of hypertonicity.
下面資料來自 uptodate
Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment
碳酸氫鹽和代謝性酸中毒 — 如果動脈 pH 值低於 6.90，我們建議使用碳酸氫鹽。如果血清鉀低於 5.3 mEq/L，我們會在 400 mL 無菌水中加入 100 mEq 碳酸氫鈉和 20 mEq氯化鉀，給藥時間超過 2 小時。
Bicarbonate and metabolic acidosis — We suggest administering bicarbonate if the arterial pH is less than 6.90. We give 100 mEq of sodium bicarbonate in 400 mL sterile water with 20 mEq of potassium chloride, if the serum potassium is less than 5.3 mEq/L, administered over two hours.
應每兩小時監測一次靜脈 pH 值和碳酸氫鹽濃度，並且可以重複碳酸氫鹽劑量，直到 pH 值升至 7.00 以上（參見下面的“監測”）。當碳酸氫鹽 (HCO3) 濃度增加時，血清 K 值可能會下降，可能需要更積極的 KCl 補充。
The venous pH and bicarbonate concentration should be monitored every two hours, and bicarbonate doses can be repeated until the pH rises above 7.00 (see 'Monitoring' below). When the bicarbonate (HCO3) concentration increases, the serum K may fall and more aggressive KCl replacement may be required.
DKA 中碳酸氫鹽治療的適應症存在爭議[ 34 ]，並且缺乏益處的證據[ 35-37 ]。在一項對 21 名入院動脈 pH 值在 6.90 至 7.14（平均 7.01）之間的 DKA 患者進行的隨機試驗中，碳酸氫鹽治療並未改變發病率或死亡率[ 35 ]。然而，該研究規模較小，僅限於動脈pH值6.90及以上的患者，碳酸氫鹽組和安慰劑組之間動脈pH值和血清碳酸氫鹽的上升率沒有差異。尚未進行有關在 pH 值低於 6.90 的 DKA 中使用碳酸氫鹽的前瞻性隨機試驗。
The indications for bicarbonate therapy in DKA are controversial [34], and evidence of benefit is lacking [35-37]. In a randomized trial of 21 DKA patients with an admission arterial pH between 6.90 and 7.14 (mean 7.01), bicarbonate therapy did not change morbidity or mortality [35]. However, the study was small, limited to patients with an arterial pH 6.90 and above, and there was no difference in the rate of rise in the arterial pH and serum bicarbonate between the bicarbonate and placebo groups. No prospective randomized trials have been performed concerning the use of bicarbonate in DKA with pH values less than 6.90.
碳酸氫鹽的給藥也存在爭議，因為除了缺乏證據證明其益處外，還存在一些潛在的有害影響： ●如果碳酸氫鹽輸注成功地增加了血液碳酸氫鹽濃度，則可以
Bicarbonate administration is also controversial because in addition to lack of evidence for benefit, there are several potential harmful effects:
減少過度換氣驅動，從而升高血液pCO2。血液 CO2 張力的增加比動脈 HCO3 的增加更快地反映在血腦屏障上。這可能會導致大腦 pH 值的反常下降。儘管神經系統惡化已歸因於這種機制，但它仍然是一個非常有爭議的效應，而且即使發生，也很少見[ 38 ]。
●If bicarbonate infusion successfully increases the blood bicarbonate concentration, this can reduce the hyperventilatory drive, which will raise the blood pCO2. Increased blood CO2 tension is more quickly reflected across the blood brain barrier than the increased arterial HCO3. This may cause a paradoxical fall in cerebral pH. Although neurologic deterioration has been attributed to this mechanism, it remains a very controversial effect and, if it occurs, is rare [38].
●服用鹼可能會減慢酮症的恢復速度[ 39,40]。在一項針對七名患者的研究中，三名接受碳酸氫鹽治療的患者血清酮酸陰離子水平升高，酮症消退延遲六小時[39 ]。動物研究表明，碳酸氫鹽輸注可以加速生酮。這被認為與酸血症對有機性酸中毒有“制動作用”有關。任何增加全身 pH 值的操作都會減弱這種制動作用 [ 35 ]。
●The administration of alkali may slow the rate of recovery of the ketosis [39,40]. In a study of seven patients, the three patients treated with bicarbonate had a rise in serum ketoacid anion levels and a six-hour delay in resolution of ketosis [39]. Animal studies indicate that bicarbonate infusion can accelerate ketogenesis. This is thought to be related to the fact that acidemia has a “braking effect” on organic acidosis. This brake is lessened by any maneuver that increases systemic pH [35].
●給予鹼可導致治療後代謝性鹼中毒，因為酮酸陰離子與胰島素的代謝會導致碳酸氫根的產生，並自發糾正大部分代謝性酸中毒。(參見“成人糖尿病酮症酸中毒和高滲性高血糖狀態：流行病學和發病機制”，關於‘陰離子間隙代謝性酸中毒’一節)
●Alkali administration can lead to a posttreatment metabolic alkalosis, since metabolism of ketoacid anions with insulin results in the generation of bicarbonate and spontaneous correction of most of the metabolic acidosis. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis", section on 'Anion gap metabolic acidosis'.)
There are, however, selected patients who may benefit from cautious alkali therapy [38]. They include:
●Patients with an arterial pH ≤6.9 in whom decreased cardiac contractility and vasodilatation can further impair tissue perfusion [41,42]. At an arterial pH above 7.00, most experts agree that bicarbonate therapy is not necessary, since therapy with insulin and volume expansion largely reverse the metabolic acidosis [43].
●Patients with potentially life-threatening hyperkalemia, since bicarbonate administration in acidemic patients may drive potassium into cells, thereby lowering the serum potassium concentration [44]. (See"Treatment and prevention of hyperkalemia in adults".)
一篇 2011 年回顧文章說. 沒有證據顯示在 DKA 給予 bicarbonate 有好處. 尤其是兒科病人. 在 pH 6.9 以下也缺乏足夠證據給予建議.
處理目標, 減少高氯酸中毒, 減少 CSF 酸化, 減少腦水腫.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224469/
Conclusions
The evidence to date does not support the use of bicarbonate administration for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical and physiological harm and the lack of clinical or sustained physiological benefits. There also is insufficient evidence to justify the recommendation of bicarbonate administration in more extreme acidemia of pH < 6.90. Future research should focus on the use of more balanced and physiological resuscitation fluids with buffering capacity, in the modern context of DKA management, with the goal of reducing the component of hyperchloremic acidosis in DKA while minimizing the risk of CSF acidosis and associated CE
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