Perioperative anesthetic management for cesarean section of a parturient with gestational diabetes insipidus

0 It is a potentially life threatening state if left untreated. We present the perioperative anesthetic management of a preterm parturient with GDI pre- senting for an urgent Cesarean section. Consent for the use of personal health information contained in this manuscript has been obtained in accordance with Duke University Medical Center Institutional Review Board guidelines 1 ESTATIONAL diabetes insipidus (GDI) is a rare endocrinopathy, occurring in approximately 4:100,000 pregnancies [Dmarche anesthsique priopratoire pour la csarienne chez une parturiente atteinte de diabte insipide gestationnel] Hector J. Lacassie MD,* Holly A. Muir MD FRCPC,* Simon Millar MBCHB FRCA, Ashraf S. Habib MBBCH MSc FRCA* Purpose: Gestational diabetes insipidus (GDI) is a rare endocrinopathy complicating about 4:100,000 deliveries. We present the case of a preterm parturient with GDI and severe hypernatremia (serum sodium concentration = 174 mmolL-1) presenting for an urgent Cesarean section. Clinical features: Fluid resuscitation and desmopressin supplementation partially corrected the patient's homeostasis, allowing us to carefully titrate epidural anesthesia for an urgent Cesarean section. After delivery, the patient was transferred to the intensive care unit. The serum sodium concentration of the mother and the neonate was normalized over 48 hr and three days respectively. Conclusion: The careful perioperative management of GDI led to a favourable outcome of the mother and fetus. - Case report A 25-yr-old parturient, G2P1 at 30 weeks gestation, presented to a community hospital with nausea, vomiting and polyuria increasing over three weeks. Medical history was significant for asthma and a family and personal history of myotonic dystrophy (MD). Symptoms of MD included bilateral ptosis and myotonic grip of the upper extremities. There were no cardiorespiratory symptoms. Initial treatment for hyperemesis included fluids and antiemetics; however, continued polyuria and increasing hypernatemia with clinical decline led to transfer to our teaching hospital. On admission the patient was contracting, therefore tocolysis was started with magnesium sulfate and terbutaline. Initial investigations revealed: Na 174 mmolL1 (normal 140 5 mmolL1), urine osmolality 133 mOsmkg1 (normal 2501200 mOsmkg1) and serum osmolality 360 mOsmkg1 (normal 285 8 mOsmkg1). Laboratory testing for pre-eclampsia TABLE Laboratory values *All pO2 measurements were under oxygen by facemask at 6 Lmin1. was negative. Other laboratory values over the perioperative period are summarized in the Table. She was drowsy but rousable and appropriately oriented, with no localizing neurological signs. On physical examination the most striking feature was her markedly swollen tongue, visibly protruding from her oral cavity. It was suggested by history that this occurred following the administration of an antibiotic at the referring centre, suggesting an allergic reaction, although there were no other signs of allergy and no signs of swelling beyond the oral cavity. Her airway examination revealed limited mouth opening with a Mallampati grade IV view due to the enlarged tongue occupying the entire oral cavity. There was no associated compromise in respiration. After a 10-mg dose of dexamethasone iv, the tongue edema improved over 90 min, leading to a change in Mallampati view from grade IV to III. Fetal cardiograph showed a lack of beat to beat variability with repetitive late decelerations. A decision was made that delivery of the fetus should proceed expeditiously by Cesarean section once the mother was stabilized. Careful resuscitation was commenced with 2 g iv 1-deamino-8-D-arginine vasopressin or desmopressin (DDAVP), and dextrose 5% at 200 mLhr1 to decrease the serum sodium concentration at a rate of approximately 1 mmolL1hr1.2 Arterial pressure and central venous pressure (CVP) monitoring was instituted to guide therapy. The baseline CVP value was 0 mmHg, blood pressure 135/55 mmHg and heart rate 110min1. The CVP increased to 4 mmHg following fluid resuscitation. A lumbar L2L3 epidural catheter was then placed for Cesarean section. Four boluses of 5 mL ropivacaine 0.5% were administered incrementally over 20 min, in addition to 75 g epidural fentanyl, with further 10 mL of lidocaine 2% to achieve a bilateral T4 sensory level. The CVP was 2 mmHg following administration of the epidural local anesthetics. The patient remained stable hemodynamically, with an oxygen saturation of 100% throughout the procedure (oxygen 6 Lmin1 was delivered by facemask). With the T4 sensory level, good surgical anesthesia was achieved. Of concern however, during the course of the operative procedure, was increasing somnolence of the mother. The woman was admitted to the intensive care unit (ICU) after delivery for further evaluation and stabilization. The serum Na concentration was 166 mmoL1 and 162 mmolL1 immediately prior to the Cesarean section and upon admission to the ICU, respectively. A male infant with Apgar scores 1, 4, 5, at one, five, and ten minutes respectively was delivered. Fetal cord blood samples revealed pH 7.13, base excess - 4, total CO2 30 mmolL1 and Na 168 mmolL1. Upon admission to the neonatal ICU, a decision to institute mechanical ventilation was made due to persistent hypotonia and poor respiratory effort. Free water was delivered to the baby and serum sodium normalized over the next three days. The neonate was weaned quickly off ventilatory support. The mothers sodium concentration was corrected by 48 hr post-delivery in the ICU. Mental state lagged behind metabolic restoration; however, neurologic studies which included a computed tomography scan were normal. On postoperative day three, the patient developed acute pancreatitis, requiring a prolonged ICU stay. She was discharged home 29 days after admission. Discussion This is the first report in the English literature describing the perioperative anesthetic management for Cesarean section of a parturient with GDI and severe hypernatremia. Diabetes insipidus is a syndrome characterized clinically by excretion of abnormally large volumes of dilute urine.3 It is caused by a dysfunction in the interaction of antidiuretic hormone, also known as arginine vasopressin (AVP) and the vasopressin receptors in the distal convoluted tubules and collecting ducts of the renal medulla,4 resulting in solute free water loss in the urine and hypernatremia. GDI results from increased metabolism of AVP.3 The pregnant state may induce Lacassie et al.: GESTATIONAL DIABETES INSIPIDUS AND ANESTHESIA diabetes insipidus or unmask previous subclinical diabetes insipidus.1 The mechanisms involved are 1) decreased renal responsiveness to AVP; 2) increased placental production of vasopressinase (a cystine aminopeptidase), with decreased availability of AVP due to four- to sixfold increased degradation by placental vasopressinase,5 3) a decrease in plasma sodium concentration by approximate (...truncated)