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Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery
International Journal of Obstetric Anesthesia (2017) xxx, xxx–xxx 0959-289X/$ - see front matter Ó 2017 Elsevier Ltd. All rights reserved. https://doi.org/10.1016/j.ijoa.2017.08.002
CASE REPORT
www.obstetanesthesia.com
Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery P. Sangwan, B. Srinivasan, S. Janweja, S. Jangid Department of Anesthesia and Intensive Care, Dr. Sampurnanand Medical College, Jodhpur 342003, India
ABSTRACT Renal tubular acidosis, associated with hypothyroidism, is rare. We present the case of a woman with known renal tubular acidosis and treated hypothyroidism who underwent emergency cesarean delivery under uneventful combined spinal-epidural anesthesia. The rationale for choosing the anesthetic technique and the potential risks associated with anesthesia and renal tubular acidosis are discussed. Ó 2017 Elsevier Ltd. All rights reserved.
Keywords: Renal tubular acidosis; Hypothyroidism; Hypokalemia; Local anesthetic; Combined spinal epidural
Introduction Renal tubular acidosis (RTA) is a term applied to a group of transport defects in the reabsorption of bicarbonate (HCO3 ), the excretion of hydrogen ion (H+), or both.1 Several subtypes of the disorder are recognized, but RTA 1 and 2 are associated with hypokalemia. Type 1 RTA is caused by impaired secretion of hydrogen ions in the distal tubule; while type 2 RTA is due to impaired bicarbonate reabsorption in the proximal renal tubule. The result of either defect is hypokalemic, non-anion gap hyperchloremic metabolic acidosis, and inadequate acidification of urine. We share our experience in the anesthetic management of an emergency cesarean delivery in a patient with adultonset distal renal tubular acidosis with hypokalemia and treated hypothyroidism.
Case report A 30-year-old woman weighing 58 kg and of height 136 cm (body mass index [BMI] 31.4 kg/m2), who had previously been diagnosed as having RTA with hypokalemia and hypothyroidism (possibly autoimmune), was admitted to our hospital on an emergency basis. During a routine obstetric visit at 36 weeks of gestational age, an abnormal fetal heart rate was detected. As fetal Accepted August 2017 Correspondence to: Dr P Sangwan, 100/4, JSI Officer’s Enclave, Near Military Hospital, Jodhpur, Rajasthan, India. E-mail address: [email protected]
hypoxia was suspected, an emergency cesarean delivery was planned. The patient had been diagnosed with hypothyroidism four years prior; and subsequently with RTA, two years later. She had been hospitalized several times owing to hypokalemia-induced quadriparetic events. At the time of admission, she was on thyroxine 150 mg once a day and sodium bicarbonate 325 mg thrice daily and potassium chloride 50 mEq/day orally. On physical examination her skin and mucosa were dry; however, her hemodynamic parameters were within the normal range. Muscle power was equal in both upper and lower limbs. Recent blood investigations revealed a normal free T3, free T4 and 25-hydroxyvitamin D and an elevated TSH of 16.2 ulU/mL (normal 0.5–5.5 uIU/mL). Immunofluorescence microscopy was positive for antinuclear antibody (ANA), while negative for anti-dsDNA antibody. Her complete blood count, coagulation parameters, liver and renal function tests were in the normal range. Her preoperative arterial blood gas (ABG) analysis (on room air) was pH 7.36, pO2 98.8 mmHg, pCO2 22.5 mmHg, HCO3 12.6 mmol/L and base deficit 10.5 mmol/L. Her electrolytes were Na+ 139 mmol/L, Cl 106 mmol/L, K+ 2.9 mmol/L, Ca+ 1.17 mmol/L and the urinary pH 6.0. The electrocardiogram was within normal limits. Recent whole abdomen ultrasonography reported a single live intrauterine fetus and normal maternal renal anatomy (no nephrocalcinosis). In the operating room, standard monitoring was attached and intravenous (IV) access was secured in both forearms using 16-gauge (G) and 18-G IV cannulae.
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002
2
Anesthetic considerations in a parturient with renal tubular acidosis
Potassium chloride (KCl) 20 mEq with dextrose 5% 50 mL infusion was started at 50 mL/h. Radial arterial cannulation was performed for continuous blood pressure monitoring and perioperative ABG analysis. A combined spinal-epidural (CSE) technique was chosen for anesthesia for surgery. With the woman in the sitting position, the epidural space was identified at the L3–4 interspace, using a loss-of-resistance technique to saline with an 18-G Tuohy needle. A 22-G epidural catheter was passed cephalad and secured to the skin at 9 cm (5 cm in the epidural space). A subarachnoid block was initiated at the L4–5 interspace, with the administration of 1.25 mL of 0.5% hyperbaric levobupivacaine and 25 lg of fentanyl via a 25-G Quincke spinal needle. The time to onset of the subarachnoid block was approximately five minutes and the highest level of the block to pinprick was T6, this being achieved within 10 minutes. During the procedure, 1500 mL of Ringer’s lactate was infused, normal saline being avoided to prevent hyperchloremic metabolic acidosis. Concomitantly with the subarachnoid block, a continuous infusion of norepinephrine was started to prevent spinal-induced hypotension. The initial dose was set at 2 mg/min, which was titrated to maintain mean arterial pressure (MAP) above 70 mmHg. A single episode of hypotension occurred 14 minutes after the intrathecal injection and was treated with a bolus of IV fluid and an increase in the norepinephrine infusion. After delivery, 3 IU of oxytocin was administered over 15 s, as requested by the surgeon. The patient remained comfortable throughout the procedure. The surgery lasted for 70 min and at completion the patient’s blood pressure was 112/74 mmHg, MAP 86 mmHg without norepinephrine support, pulse rate 78 beats/min and urine output 320 mL. The child had an Apgar score of 7 at 1-min, and after suctioning and physical stimulation, 9 at 5-min. The patient was moved to the high dependency unit for further monitoring with postoperative ABG parameters as pH-7.34, pO2-77.8 mmHg, pCO2-27.6 mmHg, HCO3-14.6 mmol/L, base deficit 9.6 mmol/L and electrolytes as Na+ 145.8 mmol/L, Cl-108 mmol/L, K+ 3.73 mmol/L and Ca+ 1.08 mmol/L. Her electrolytes were Na+ 146 mmol/L, Cl 108 mmol/L, K+ 3.7 mmol/L, and Ca+ 1.1 mmol/L. After the spinal block wore off, a continuous epidural infusion of ropivacaine 0.25% was started at 6 mL/h. This was to provide postoperative analgesia and to prevent pain-related hyperventilation, which could further decrease the serum bicarbonate level. Her usual medications were started the following morning and the patient and her baby were discharged home on the sixth postpartum day.
Discussion Providing anesthesia to patients with RTA can be challenging. Our patient had a history of RTA and
hypokalemia and had required hospitalization for hypokalemic-paralysis. After balancing the risks and benefits of general anesthesia versus neuraxial anesthesia, we chose a combined spinal-epidural anesthetic for her cesarean delivery. Renal tubular acidosis is a constellation of syndromes, arising from different derangements of tubular acid transport. Distal RTA is one of the leading causes of secondary paralysis, and consists of hypokalemia, hyperchloremic metabolic acidosis, inability to lower urine pH below 5.5 in the presence of systemic acidosis, nephrocalcinosis and nephrolithiasis.1 Renal tubular acidosis type I is either inherited or acquired. In the acquired form, the disorder can be caused by drugs, autoimmune diseases or infection.1 Although the exact mechanism remains unclear, the concurrence of RTA and autoimmune disease is well documented, especially with diseases such as Sjogren’s syndrome and systemic lupus erythematosus (SLE).1 An autoimmune etiology causes dysfunction of various transporters and cotransporters involved in acidification in the renal tubular system.2 Renal tubular acidosis has been reported rarely in patients with thyroid dysfunction, for example hyperthyroidism, Hashimoto’s thyroiditis and hypothyroidism.3 The acidification defect has been related to thyroxine deficiency.4,5 Thyroid hormones modulate the response to an acid challenge, alter the expression of several key acid-base transporters, and increase the cell membrane Na+ K+ ATP-ase pumps. In hypothyroidism, the content and function of these pumps is reduced, causing a decreased elimination of H+ ions.6 This will exacerbate the acidotic state caused by RTA. In our patient, we were unable to confirm an autoimmune cause, other than hypothyroidism, as confirmatory tests for other etiologies were not done. Acidosis and hypokalemia, which accompany RTA, have pharmacodynamic and pharmacokinetic implications for both general and neuraxial anesthesia. During general anesthesia, acidosis leads to an exaggerated hypotensive response to inhalational and IV drugs and to positive pressure ventilation.7 Acidosis and hypokalemia also delay recovery from neuromuscular blockade, with an increased risk of postoperative residual muscle weakness,8 especially in hypothyroid patients. Neuraxial techniques for anesthesia and postoperative analgesia should minimise respiratory depression and muscle weakness due to general anesthetics, opioids, and neuromuscular blockers. However, if the pH is reduced, systemic vascular resistance may decrease9 and the response to vasopressors and inotopes can remain suboptimal. Thus, these patients may be more prone to hemodynamic instability during neuraxial anesthesia. In one study, hypothyroid animals had a diminished response to phenylephrine and other a-1 adrenergic drugs.10 Polikar et al. found an improved response to phenylephrine once hypothyroid patients
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002
P. Sangwan et al. were treated.11 Although our patient had normal thyroid function, due to thyroxine therapy, we used a norepinephrine infusion, rather than phenylephrine, titrated to the MAP to prevent hypotension. Norepinephrine was chosen due to its greater affinity for b-1 receptors. The threshold for central nervous toxicity due to local anesthetics is potentially reduced in pregnancy due to the hyperdynamic circulation, decreased protein binding and exaggerated lumbar lordosis.12 In acidotic patients, there is a greater potential for local anesthetic systemic toxicity as well.13 Since bupivacaine has a greater propensity to cause toxicity, a ropivacaine infusion was administered epidurally for postoperative analgesia. This technique also allowed us to avoid nonsteroidal anti-inflammatory drugs, which can cause renal injury.14
Conclusion In summary, we report the anesthetic management of a parturient with renal tubular acidosis, hypokalemia and treated hypothyroidism, undergoing cesarean delivery. The use of a combined spinal-epidural technique and a prophylactic infusion of norepinephrine to prevent hypotension resulted in a successful outcome.
References 1. Rodrı´guez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol 2002;13:2160–70.
3 2. Koul PA, Wahid A. Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism. Saudi J Kidney Dis Transpl 2011;22:1014–6. 3. Yoshioka H, Yamazaki H, Yasumura R, Wada K, Kobayashi Y. Anesthetic management of a surgical patient with chronic renal tubular acidosis complicated by subclinical hypothyroidism. Case Rep Anesthesiol 2016;2016:2434381. 4. Michael UF, Chavez R, Cookson SL, Vaamonde CA. Impaired urinary acidification in the hypothyroid rat. Pflugers Arch 1976;361:215–20. 5. Drukker A, Dolberg M, Landau H. Renal tubular acidosis in a patient with hypothyroidism due to autoimmune thyroiditis – improvement with hormone replacement therapy. Int J Pediatr Nephrol 1982;3:205–9. 6. Garg LC, Tisher CC. Effects of thyroid hormone on Na-K adenosine triphosphatase activity along the rat nephron. J Lab Clin Med 1985;106:568–72. 7. Barash PG, Cullen BF, Stoelting RK, et al. Acid base, fluids and electrolytes. 5th ed. Philadelphia: Lippincott Williams Wilkins; 2006. 8. Sinclair R, Faleiro R. Delayed recovery of consciousness after anaesthesia. Contin Educ Anaesth Crit Care Pain 2006;3:114–8. 9. Lim S. Metabolic acidosis. Acta Med Indones 2007;39:145–50. 10. Vargas F, Moreno JM, Rodrıguez Gomez I, et al. Vascular and renal function in experimental thyroid disorders. Eur J Endocrinol 2006;154:197–212. 11. Polikar R, Kennedy B, Ziegler M, Smith J, Nicod P. Decreased sensitivity to a-adrenergic stimulation in hypothyroid patients. J Clin Endocrinol Metab 1990;70:1761–4. 12. Datta S, Kodali BS, Segal S (eds). Ch. 3. Perinatal pharmacology. In: Obstetric Anesthesia Handbook, 5th ed. Springer, 2010;3:30–3. 13. Ciechanowicz S, Patil V. Lipid emulsion for local anesthetic systemic toxicity. Anesthesiol Res Pract 2012;2012:131784. 14. Ejaz P, Bhojani K, Joshi VR. NSAIDs and kidney. J Assoc Physicians India 2004;52:632–40.
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002
CASE REPORT
www.obstetanesthesia.com
Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery P. Sangwan, B. Srinivasan, S. Janweja, S. Jangid Department of Anesthesia and Intensive Care, Dr. Sampurnanand Medical College, Jodhpur 342003, India
ABSTRACT Renal tubular acidosis, associated with hypothyroidism, is rare. We present the case of a woman with known renal tubular acidosis and treated hypothyroidism who underwent emergency cesarean delivery under uneventful combined spinal-epidural anesthesia. The rationale for choosing the anesthetic technique and the potential risks associated with anesthesia and renal tubular acidosis are discussed. Ó 2017 Elsevier Ltd. All rights reserved.
Keywords: Renal tubular acidosis; Hypothyroidism; Hypokalemia; Local anesthetic; Combined spinal epidural
Introduction Renal tubular acidosis (RTA) is a term applied to a group of transport defects in the reabsorption of bicarbonate (HCO3 ), the excretion of hydrogen ion (H+), or both.1 Several subtypes of the disorder are recognized, but RTA 1 and 2 are associated with hypokalemia. Type 1 RTA is caused by impaired secretion of hydrogen ions in the distal tubule; while type 2 RTA is due to impaired bicarbonate reabsorption in the proximal renal tubule. The result of either defect is hypokalemic, non-anion gap hyperchloremic metabolic acidosis, and inadequate acidification of urine. We share our experience in the anesthetic management of an emergency cesarean delivery in a patient with adultonset distal renal tubular acidosis with hypokalemia and treated hypothyroidism.
Case report A 30-year-old woman weighing 58 kg and of height 136 cm (body mass index [BMI] 31.4 kg/m2), who had previously been diagnosed as having RTA with hypokalemia and hypothyroidism (possibly autoimmune), was admitted to our hospital on an emergency basis. During a routine obstetric visit at 36 weeks of gestational age, an abnormal fetal heart rate was detected. As fetal Accepted August 2017 Correspondence to: Dr P Sangwan, 100/4, JSI Officer’s Enclave, Near Military Hospital, Jodhpur, Rajasthan, India. E-mail address: [email protected]
hypoxia was suspected, an emergency cesarean delivery was planned. The patient had been diagnosed with hypothyroidism four years prior; and subsequently with RTA, two years later. She had been hospitalized several times owing to hypokalemia-induced quadriparetic events. At the time of admission, she was on thyroxine 150 mg once a day and sodium bicarbonate 325 mg thrice daily and potassium chloride 50 mEq/day orally. On physical examination her skin and mucosa were dry; however, her hemodynamic parameters were within the normal range. Muscle power was equal in both upper and lower limbs. Recent blood investigations revealed a normal free T3, free T4 and 25-hydroxyvitamin D and an elevated TSH of 16.2 ulU/mL (normal 0.5–5.5 uIU/mL). Immunofluorescence microscopy was positive for antinuclear antibody (ANA), while negative for anti-dsDNA antibody. Her complete blood count, coagulation parameters, liver and renal function tests were in the normal range. Her preoperative arterial blood gas (ABG) analysis (on room air) was pH 7.36, pO2 98.8 mmHg, pCO2 22.5 mmHg, HCO3 12.6 mmol/L and base deficit 10.5 mmol/L. Her electrolytes were Na+ 139 mmol/L, Cl 106 mmol/L, K+ 2.9 mmol/L, Ca+ 1.17 mmol/L and the urinary pH 6.0. The electrocardiogram was within normal limits. Recent whole abdomen ultrasonography reported a single live intrauterine fetus and normal maternal renal anatomy (no nephrocalcinosis). In the operating room, standard monitoring was attached and intravenous (IV) access was secured in both forearms using 16-gauge (G) and 18-G IV cannulae.
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002
2
Anesthetic considerations in a parturient with renal tubular acidosis
Potassium chloride (KCl) 20 mEq with dextrose 5% 50 mL infusion was started at 50 mL/h. Radial arterial cannulation was performed for continuous blood pressure monitoring and perioperative ABG analysis. A combined spinal-epidural (CSE) technique was chosen for anesthesia for surgery. With the woman in the sitting position, the epidural space was identified at the L3–4 interspace, using a loss-of-resistance technique to saline with an 18-G Tuohy needle. A 22-G epidural catheter was passed cephalad and secured to the skin at 9 cm (5 cm in the epidural space). A subarachnoid block was initiated at the L4–5 interspace, with the administration of 1.25 mL of 0.5% hyperbaric levobupivacaine and 25 lg of fentanyl via a 25-G Quincke spinal needle. The time to onset of the subarachnoid block was approximately five minutes and the highest level of the block to pinprick was T6, this being achieved within 10 minutes. During the procedure, 1500 mL of Ringer’s lactate was infused, normal saline being avoided to prevent hyperchloremic metabolic acidosis. Concomitantly with the subarachnoid block, a continuous infusion of norepinephrine was started to prevent spinal-induced hypotension. The initial dose was set at 2 mg/min, which was titrated to maintain mean arterial pressure (MAP) above 70 mmHg. A single episode of hypotension occurred 14 minutes after the intrathecal injection and was treated with a bolus of IV fluid and an increase in the norepinephrine infusion. After delivery, 3 IU of oxytocin was administered over 15 s, as requested by the surgeon. The patient remained comfortable throughout the procedure. The surgery lasted for 70 min and at completion the patient’s blood pressure was 112/74 mmHg, MAP 86 mmHg without norepinephrine support, pulse rate 78 beats/min and urine output 320 mL. The child had an Apgar score of 7 at 1-min, and after suctioning and physical stimulation, 9 at 5-min. The patient was moved to the high dependency unit for further monitoring with postoperative ABG parameters as pH-7.34, pO2-77.8 mmHg, pCO2-27.6 mmHg, HCO3-14.6 mmol/L, base deficit 9.6 mmol/L and electrolytes as Na+ 145.8 mmol/L, Cl-108 mmol/L, K+ 3.73 mmol/L and Ca+ 1.08 mmol/L. Her electrolytes were Na+ 146 mmol/L, Cl 108 mmol/L, K+ 3.7 mmol/L, and Ca+ 1.1 mmol/L. After the spinal block wore off, a continuous epidural infusion of ropivacaine 0.25% was started at 6 mL/h. This was to provide postoperative analgesia and to prevent pain-related hyperventilation, which could further decrease the serum bicarbonate level. Her usual medications were started the following morning and the patient and her baby were discharged home on the sixth postpartum day.
Discussion Providing anesthesia to patients with RTA can be challenging. Our patient had a history of RTA and
hypokalemia and had required hospitalization for hypokalemic-paralysis. After balancing the risks and benefits of general anesthesia versus neuraxial anesthesia, we chose a combined spinal-epidural anesthetic for her cesarean delivery. Renal tubular acidosis is a constellation of syndromes, arising from different derangements of tubular acid transport. Distal RTA is one of the leading causes of secondary paralysis, and consists of hypokalemia, hyperchloremic metabolic acidosis, inability to lower urine pH below 5.5 in the presence of systemic acidosis, nephrocalcinosis and nephrolithiasis.1 Renal tubular acidosis type I is either inherited or acquired. In the acquired form, the disorder can be caused by drugs, autoimmune diseases or infection.1 Although the exact mechanism remains unclear, the concurrence of RTA and autoimmune disease is well documented, especially with diseases such as Sjogren’s syndrome and systemic lupus erythematosus (SLE).1 An autoimmune etiology causes dysfunction of various transporters and cotransporters involved in acidification in the renal tubular system.2 Renal tubular acidosis has been reported rarely in patients with thyroid dysfunction, for example hyperthyroidism, Hashimoto’s thyroiditis and hypothyroidism.3 The acidification defect has been related to thyroxine deficiency.4,5 Thyroid hormones modulate the response to an acid challenge, alter the expression of several key acid-base transporters, and increase the cell membrane Na+ K+ ATP-ase pumps. In hypothyroidism, the content and function of these pumps is reduced, causing a decreased elimination of H+ ions.6 This will exacerbate the acidotic state caused by RTA. In our patient, we were unable to confirm an autoimmune cause, other than hypothyroidism, as confirmatory tests for other etiologies were not done. Acidosis and hypokalemia, which accompany RTA, have pharmacodynamic and pharmacokinetic implications for both general and neuraxial anesthesia. During general anesthesia, acidosis leads to an exaggerated hypotensive response to inhalational and IV drugs and to positive pressure ventilation.7 Acidosis and hypokalemia also delay recovery from neuromuscular blockade, with an increased risk of postoperative residual muscle weakness,8 especially in hypothyroid patients. Neuraxial techniques for anesthesia and postoperative analgesia should minimise respiratory depression and muscle weakness due to general anesthetics, opioids, and neuromuscular blockers. However, if the pH is reduced, systemic vascular resistance may decrease9 and the response to vasopressors and inotopes can remain suboptimal. Thus, these patients may be more prone to hemodynamic instability during neuraxial anesthesia. In one study, hypothyroid animals had a diminished response to phenylephrine and other a-1 adrenergic drugs.10 Polikar et al. found an improved response to phenylephrine once hypothyroid patients
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002
P. Sangwan et al. were treated.11 Although our patient had normal thyroid function, due to thyroxine therapy, we used a norepinephrine infusion, rather than phenylephrine, titrated to the MAP to prevent hypotension. Norepinephrine was chosen due to its greater affinity for b-1 receptors. The threshold for central nervous toxicity due to local anesthetics is potentially reduced in pregnancy due to the hyperdynamic circulation, decreased protein binding and exaggerated lumbar lordosis.12 In acidotic patients, there is a greater potential for local anesthetic systemic toxicity as well.13 Since bupivacaine has a greater propensity to cause toxicity, a ropivacaine infusion was administered epidurally for postoperative analgesia. This technique also allowed us to avoid nonsteroidal anti-inflammatory drugs, which can cause renal injury.14
Conclusion In summary, we report the anesthetic management of a parturient with renal tubular acidosis, hypokalemia and treated hypothyroidism, undergoing cesarean delivery. The use of a combined spinal-epidural technique and a prophylactic infusion of norepinephrine to prevent hypotension resulted in a successful outcome.
References 1. Rodrı´guez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol 2002;13:2160–70.
3 2. Koul PA, Wahid A. Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism. Saudi J Kidney Dis Transpl 2011;22:1014–6. 3. Yoshioka H, Yamazaki H, Yasumura R, Wada K, Kobayashi Y. Anesthetic management of a surgical patient with chronic renal tubular acidosis complicated by subclinical hypothyroidism. Case Rep Anesthesiol 2016;2016:2434381. 4. Michael UF, Chavez R, Cookson SL, Vaamonde CA. Impaired urinary acidification in the hypothyroid rat. Pflugers Arch 1976;361:215–20. 5. Drukker A, Dolberg M, Landau H. Renal tubular acidosis in a patient with hypothyroidism due to autoimmune thyroiditis – improvement with hormone replacement therapy. Int J Pediatr Nephrol 1982;3:205–9. 6. Garg LC, Tisher CC. Effects of thyroid hormone on Na-K adenosine triphosphatase activity along the rat nephron. J Lab Clin Med 1985;106:568–72. 7. Barash PG, Cullen BF, Stoelting RK, et al. Acid base, fluids and electrolytes. 5th ed. Philadelphia: Lippincott Williams Wilkins; 2006. 8. Sinclair R, Faleiro R. Delayed recovery of consciousness after anaesthesia. Contin Educ Anaesth Crit Care Pain 2006;3:114–8. 9. Lim S. Metabolic acidosis. Acta Med Indones 2007;39:145–50. 10. Vargas F, Moreno JM, Rodrıguez Gomez I, et al. Vascular and renal function in experimental thyroid disorders. Eur J Endocrinol 2006;154:197–212. 11. Polikar R, Kennedy B, Ziegler M, Smith J, Nicod P. Decreased sensitivity to a-adrenergic stimulation in hypothyroid patients. J Clin Endocrinol Metab 1990;70:1761–4. 12. Datta S, Kodali BS, Segal S (eds). Ch. 3. Perinatal pharmacology. In: Obstetric Anesthesia Handbook, 5th ed. Springer, 2010;3:30–3. 13. Ciechanowicz S, Patil V. Lipid emulsion for local anesthetic systemic toxicity. Anesthesiol Res Pract 2012;2012:131784. 14. Ejaz P, Bhojani K, Joshi VR. NSAIDs and kidney. J Assoc Physicians India 2004;52:632–40.
Please cite this article in press as: Sangwan P et al. Anesthetic considerations in a parturient with renal tubular acidosis and hypothyroidism undergoing cesarean delivery. Int J Obstet Anesth (2017), https://doi.org/10.1016/j.ijoa.2017.08.002