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| CASE REPORT |
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| Year : 2017 | Volume
: 18
| Issue : 2 | Page : 73-77 |
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Nephrotic syndrome and Obstetric anesthesia
Vijay Kumar Nagpal, Uma Hariharan, Nikhil Bhasin, Rajesh Sood
Department of Anaesthesiology and Intensive Care, Dr. Ram Manohar Lohia Hospital, Postgraduate Institute of Medical Education and Research, New Delhi, India
| Date of Submission | 01-Oct-2017 |
| Date of Acceptance | 07-Nov-2017 |
| Date of Web Publication | 12-Dec-2017 |
Correspondence Address:
Dr. Uma Hariharan
BH 41, East Shalimar Bagh, New Delhi - 110 088
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/TheIAForum.TheIAForum_32_17
Renal disorders in pregnancy can be both difficult to diagnose and manage. They are associated with poor maternal and/or fetal outcomes. In pregnancy, proteinuria is common and can range from mild urinary protein elevations to nephrotic levels. The diagnosis of nephrotic syndrome (NS) can be challenging, especially in pregnancy as it can be confused with preeclampsia. NS has an incidence of 0.012%–0.025% in pregnant women. It is diagnosed by the presence of more than 3 g/day of proteins in urine, serum albumin <30 g/dL, generalized edema, hypercholesterolemia, and lipiduria. Proteinuria with hypertension is characterized by the presence of hematuria, red cell casts, raised serum creatinine, and features suggestive of systemic disease. Other causes of proteinuria include preeclampsia, diabetes mellitus (Type 1 and Type 2), Immunoglobulin A nephropathy (Ig A glomerulonephritis), focal and segmental glomerulosclerosis, and lupus nephritis. The maternal risks of NS include acute kidney insult, chronic renal failure, gestational hypertension, preeclampsia, and complications due to hypoalbuminemia. Fetal considerations in NS include fetal growth retardation, prematurity, stillbirth, fetal anasarca, and polyhydramnios. Preconception counseling and immunosuppressive drug therapy can improve overall fetomaternal outcome. We hereby present a unique case of successful anesthetic management of NS in a parturient along with concurrent hypothyroidism and hypertension, for elective cesarean section.
Keywords: Nephrotic syndrome, obstetric anesthesia, Hypothyroidism proteinuria
How to cite this article:
Nagpal VK, Hariharan U, Bhasin N, Sood R. Nephrotic syndrome and Obstetric anesthesia. Indian Anaesth Forum 2017;18:73-7 |
| Introduction | |  |
Nephrotic-range proteinuria with hypertension in early pregnancy is an indicator toward native renal disease rather than preeclampsia.[1] Prompt diagnosis and proper management of this condition are vital for maternal and fetal health. Anesthetic management of such a parturient can be challenging due to the various perioperative implications of nephrotic syndrome (NS),[2] including hypoproteinemia, antithrombin-III deficiency, airway edema, hyperlipidemia, coagulopathy, and cardiomyopathy. These can be further compounded by other concurrent diseases such as hypothyroidism and hypertension, as was the case in our patient.
| Case Report | | |
A 24-year-old, second gravida (Gravida2, Para1, Live1), female patient presented to our hospital at the 33-week period of gestation, with generalized swelling of the entire body. She was a known hypothyroid, on regular thyroxine replacement therapy since the 12th week of current pregnancy (tablet levothyroxine 75 μg once a day). She was not a booked antenatal case, and she was referred to us from a rural primary health center due to nonsubsidence of generalized anasarca and development of ascites with mild pleural and pericardial effusion at the end of second trimester on a routine abdominal scan.
On admission, the patient was advised urine routine-microscopy examination, 24-h urinary protein, renal function tests, serum electrolytes, liver function tests, and thyroid function tests. She was put on high-protein diet and on tablets iron, calcium, and levothyroxine (75 μg daily). A nephrology opinion was also sought, who advised immune marker investigations like anti-phospholipid antibody, antinuclear antibodies against deoxyribonucleic acid (Anti-ds DNA), antineutrophil cytoplasmic antibody, anticardiolipin and lupus anticoagulant, all of which were negative. A renal biopsy was not taken as the patient did not give consent. Other investigations such as coagulation profile (Prothrombin Time, Activated Partial Thromboplastin Time, and International Normalized Ratio) and lipid profile was within normal limits. On the advice of the nephrologists and the obstetric team, the patient was put on oral tablet Prednisolone 60 mg once daily and tablet aspirin 75 mg once daily. Strict input-output charting was followed. All her routine investigations were found to be normal, except for a raised thyroid-stimulating hormone level (10 U/ml) and low serum albumin levels. The dose of thyroxine replacement therapy was increased to 150 μg daily.
On physical examination, her sensorium and vital parameters were normal, except for a raised blood pressure (BP) (140/100 mmHg, recorded on three separate occasions). She was put on tablet labetalol (a combined alpha + beta-adrenergic receptor blocker) 100 mg twice daily (BD) for the same, which controlled her BP well. Dietary protein supplements were given in view of the low albumin (1.9 g/dL) and total protein levels (4.41 g/dL). In addition, the patient was started on injection (salt-poor) human Albumin (20%) 100 ml daily for 3 days, after nephrology and cardiology opinion.
An elective cesarean delivery was planned at the beginning of 37-week period of gestation in view of the previous operative delivery. A repeat ultrasound scan was done before surgery, which did not show any signs of pleural or pericardial effusion or ascites, with normal fetal well-being. Patient's blood investigation profile has been provided in [Table 1]. An ophthalmological examination revealed a normal fundoscopy.
Anesthetic management
The patient was shifted to the operating room in the left lateral position after the usual early morning dose of thyroxine replacement and antihypertensive therapy. All standard monitors were attached (Pulse oximeter, Heart rate [HR], electrocardiogram, noninvasive BP, Foleys catheter, and Temperature probe). Patient's preoperative vitals were as follows: BP-130/70 mmHg, HR-90 beats/min, oxygen saturation 100% on room air, electrocardiography was normal, respiratory rate-16/min, and temperature was 37° C. Two 18-G intravenous lines were secured in the upper limb for crystalloid fluid coloading. A decision to give regional anesthesia for cesarean delivery was taken after aspiration prophylaxis. Under local anesthesia and complete asepsis, left radial artery, and right internal jugular vein were cannulated, using standard Seldinger technique and connected to pressure monitoring transducers. Under all aseptic precautions, subarachnoid neuraxial block was performed using 1.8 ml of 0.5% bupivacaine hydrochloride (heavy) along with 10 mcg of fentanyl (opioid) in the left lateral position using 26-G Quincke needle. Block level upto T6 dermatome was achieved. There were no significant changes in the vitals after the neuraxial block (BP and pulse within 20% of preoperative baseline). Induction delivery interval was 12 min, and a live baby was successfully delivered with normal APGAR scores. Oxytocin injection was administered after cord clamping (20 IU infused in 500 ml of Ringer lactate solution). There was no episode of intraoperative hypotension, and all vital parameters were maintained within normal range throughout the procedure. The arterial blood gas analysis also showed normal values. A goal-directed intravenous fluid therapy was given according to the vital parameters (heart rate, central venous pressures [CVPs], and urine output). The CVP was kept in the range of 6–8 mmHg and urine output were maintained above 0.5–1 ml/kg/h. The total procedure time was 57 min, with an approximate blood loss of 700 ml. Postoperative pain relief was accomplished by bilateral TAP (transversus plane block) block with local anesthetic solution (0.25% Bupivacaine hydrochloride) and intravenous paracetamol infusion (1 g, 6 hourly). The patient was intensely monitored in the postanesthesia care unit for 6 h and then shifted to a high-dependency unit for overnight observation, before shifting to the ward after 24 h in a stable condition. Vital signs were stable and consistent with age and preoperative baseline (Remained within 20% of the baseline). The complete resolution of motor and sensory blockade took place within 6 h. There were no complains of nausea and vomiting at the time of discharge. No complications which are associated with subarachnoid block were observed in our patient. CVP and arterial lines were removed before discharging the patient to ward.
| Discussion | | |
Renal diseases in pregnancy can lead to a host of peripartum complications such as preeclampsia, fetal loss, intrauterine growth retardation, preterm delivery, and prematurity.[3] In most instances, a timely diagnosis with a renal biopsy can clinch the diagnosis and guide appropriate therapy after knowing the specific renal pathology. In our case, a nephrology opinion was taken and the patient did not consent for the procedure due to the fear of pregnancy loss and due to the inability to lie prone in advanced pregnancy.
Our patient also had hypertension, which was diagnosed only in the third trimester, on referral to our center, which responded well to medical management. The similarity between NS and pregnancy-induced hypertension (PIH) has resulted in either misdiagnosis or under-reporting of the existence of NS in pregnancy.[4]
NS is a less common cause of proteinuria (incidence of NS is 0.012%–0.025% of all pregnancies)[5] as compared to PIH (incidence of PIH is 3% and of eclampsia is 0.1%). The usual causes of NS in pregnancy are preeclampsia, glomerulonephritis, diabetes mellitus, renal vein thrombosis, amyloidosis, systemic lupus erythematosus,[6] and Ig-A nephropathy.[7] The diagnostic criteria [8] for NS are listed in [Table 2]. In several instances, it is imperative to treat NS with steroids. Occasionally, NS may not respond to steroids, leading to increased fetomaternal complications. This management dilemma requires a renal biopsy to know the histology of renal disease and guide therapy.
Physiological changes in pregnancy can mimic exacerbation of the disease and pose a diagnostic challenge. During normal pregnancy, physiological urinary protein excretion is increased to 300 mg/day.[9] Development of NS can further reduce serum albumin levels and cause fluid retention. Reduced serum albumin levels are also associated with low-birth-weight babies and poor fetal outcomes.[10]
Hypoproteinemia affects the delicate balance between hydrostatic and colloid osmotic pressure leading to increased loss of fluid from the capillaries, promoting the development of pulmonary edema, pleural effusion, pericardial effusion, and ascites.
Complications of NS [11] are divided into two categories: disease-associated and drug-related complications. Disease-associated complications include infections (peritonitis, sepsis, cellulitis), thromboembolism (venous thromboembolism and pulmonary embolism), hypovolemic crisis (abdominal pain, tachycardia, and hypotension), cardiovascular problems (hyperlipidemia), acute renal failure, anemia, and such as hypothyroidism, hypocalcemia, bone disease, and intussusception. Most complications originate from the large loss of plasma proteins.
Therapy for NS in pregnancy has additional maternal and fetal problems.[12] High dose steroid therapy (Prednisolone >20 mg/day) and immunosuppressive medications can cause biventricular hypertrophy, systolic anterior motion of the mitral valve, vitiation of glycemic control, increased propensity for infections, and osteoporotic bone loss.
There are several schools of thought regarding the need, timing, and risks of renal biopsy during pregnancy.[13] Although renal biopsy in pregnancy does not entail increased risks, it is infrequently performed in early and late gestation periods. Sudden renal insufficiency or massive NS of unknown origin occurring during the last few months of pregnancy are some indications for renal biopsy. Normotensive pregnant women with mild or moderate proteinuria as well as those with well-preserved renal function along with asymptomatic hematuria (microscopic) should be monitored closely, and biopsy should be deferred to the postpartum period.[14]
The general complications [8] of adult NS reported in literature include the development of generalized and pulmonary edema due to hypoalbuminemia, thrombogenesis, acute kidney injury, and renal failure. The primary abnormality is the increased glomerular permeability to albumin and other plasma proteins, causing decreased oncotic pressure, extravasation of fluid into the interstitial space, and renal sodium retention. Hypercoagulability is multifactorial, resulting from the loss of coagulation factors and a hemostatic shift toward a prothrombotic state. Renal injury is a rare complication due to edema and proteinuria and can coexist with both nephrotic and nephritic syndromes.
All the modern inhalational anesthetics such as isoflurane, desflurane, enflurane and halothane are suitable in patients with mild-to-moderate renal disease. It has also been observed that renal blood flow is maintained with isoflurane, desflurane and halothane.[8] Hypoproteinemia is the major concern during anesthetic management in NS, as the available binding sites for intravenous anesthetics are decreased in hypoalbuminemia. As thiopentone and benzodiazepines extensively bind to albumin, their free fraction is increased and a greater proportion of the administered drug reaches to the receptor sites.[15] Their metabolites are also pharmacologically active and so potentiate their clinical effect. However, dose recommendations are not available in the literature. Although free fraction of fentanyl, alfentanil, propofol, and etomidate is increased, no delay in recovery after administration is expected, due to lack of free metabolites and short redistribution of these agents. Therefore, these agents appear to be a better choice in patients with hypoalbuminemia.[16]
Along with diuretic therapy, a short-term use of 25% albumin is appropriate for some patients with acute severe peripheral or pulmonary edema who have failed diuretic therapy. Judicious albumin administration also appears to exert protective effects on the kidney by inhibition of apoptosis and scavenging of reactive oxygen species.[17]
Prolonged corticosteroid therapy may lead to several complications,[18] including precipitation of sodium and fluid retention, potassium loss, increase in BP, and blood sugar levels and also increases the susceptibility for infections, thromboembolism, and impaired wound healing. Therefore, perioperative monitoring should include BP, blood sugar, body weight, and serum electrolytes. Patients on chronic steroid therapy may require prolonged postoperative mechanical ventilation and likely to suffer from atrial arrhythmias. Perioperatively steroid therapy should be continued to avoid the hemodynamic instability.[19]
| Conclusions | | |
Perianesthetic management in obstetric NS must focus on the following issues: renal protection; hypoproteinemia management; maintaining fluid-electrolyte balance; considerations with corticosteroid therapy; and preserving the uteroplacental blood flow. Maintaining a delicate balance between adequate hydration and preventing overhydration, avoidance of nephrotoxic agents (such as nonsteroidal anti-inflammatory drugs or NSAID's, aminoglycoside antibiotics), and goal-directed fluid therapy can go a long way in ensuring a positive fetomaternal outcome. The concurrent presence of hypothyroidism and hypertension with NS can the make the situation more challenging for the obstetric anesthesiologist.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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[Table 1], [Table 2]
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