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  Table of Contents 
Year : 2021  |  Volume : 22  |  Issue : 1  |  Page : 91-93

Anesthetic management of a parturient with Wernicke's encephalopathy secondary to hyperemesis gravidarum for cesarean section

Department of Anesthesia, Maulana Azad Medical College, New Delhi, India

Date of Submission29-Feb-2020
Date of Decision22-Aug-2020
Date of Acceptance29-Aug-2020
Date of Web Publication22-Feb-2021

Correspondence Address:
Dr. Divya Gahlot
D-55 Arya Nagar Apartments, I P Extension, Patparganj, New Delhi - 110 092
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/TheIAForum.TheIAForum_18_20

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Wernicke's encephalopathy (WE) secondary to hyperemesis gravidarum (HG) is a rare but a known complication. A delay in diagnosis and treatment often results in long-term neurological sequelae. Critical care management of these patients is reported in the literature, but their anesthetic management for cesarean section is lacking. We report the case of a 28-year-old parturient who presented with HG in the first trimester of pregnancy and was managed conservatively. She later developed nystagmus, weakness, and cognitive dysfunction, and a diagnosis of WE secondary to HG was established. The patient was later posted for cesarean section in view of persistent quadriparesis and cognitive impairment at term gestation. General anesthesia was the preferred anesthesia technique of choice. Obstetric patients with preexisting neurological disease for cesarean section become a special subpopulation for anesthesiologists with their unique anesthetic challenges.

Keywords: Anesthesia, cesarean section, hyperemesis gravidarum, Wernicke's encephalopathy

How to cite this article:
Gahlot D, Agarwal M, Budoo MS, Prasad N, Singh K. Anesthetic management of a parturient with Wernicke's encephalopathy secondary to hyperemesis gravidarum for cesarean section. Indian Anaesth Forum 2021;22:91-3

How to cite this URL:
Gahlot D, Agarwal M, Budoo MS, Prasad N, Singh K. Anesthetic management of a parturient with Wernicke's encephalopathy secondary to hyperemesis gravidarum for cesarean section. Indian Anaesth Forum [serial online] 2021 [cited 2021 May 10];22:91-3. Available from: http://www.theiaforum.org/text.asp?2021/22/1/91/309832

  Introduction Top

Hyperemesis gravidarum (HG) is defined as excessive nausea and vomiting associated with pregnancy, resulting in >5% loss of prepregnancy weight.[1] It can result in various complications such as electrolyte imbalances, ketosis, dehydration, and nutritional deficiencies.[1] Anesthetic management of parturients with Wernicke's encephalopathy (WE) is not reported in literature. These patients become a special subpopulation with unique anesthetic challenges.

We report a case of a parturient who presented with WE due to HG in her first trimester of pregnancy and was later posted for cesarean section.

  Case Report Top

A 28-year-old female G5P2L0A2 presented to the antenatal clinic at 6 weeks of gestation with complaints of repeated episodes of vomiting (30–40/day) for the past 4–5 days. On examination, she was conscious and oriented with signs of dehydration (tachycardia, decreased urine output, and hypotension). A diagnosis of HG was made, and treatment was started with antiemetics and dextrose-containing intravenous (IV) fluid. She was also diagnosed with hyperthyroidism (thyroid-stimulating hormone = 0.0003 uIU/ml, anti-thyroid peroxidase [TPO] negative) and started on oral propylthiouracil. The intensity of vomiting gradually reduced; she was discharged after 2 months. One week later, the patient presented with weakness in the lower limbs for 1 day, which progressed to involve the upper limbs over a period of 3 weeks, rendering her bedridden. She also had complaints of cotton wool and electric-like sensation in the lower limbs. She had associated behavioral symptoms and memory loss. There was no bladder or bowel involvement, radicular pain, cranial nerve involvement, seizure, and headache. Neurological examination showed evoked horizontal gaze nystagmus, Mini–Mental State Examination score of 18/28, bilateral lower limb power of 1/5, upper limb power of 2/5, reduced touch, pinprick, proprioception up to T-10 dermatomal level, and areflexia. Nerve conduction studies showed delayed conduction in the motor as well as sensory nerves. Magnetic resonance imaging (MRI) brain and spine were normal. A clinical diagnosis of Guillain–Barre syndrome (GBS) was made, and IV immunoglobulins were started, but she had no significant clinical improvement. Later, cerebrospinal fluid findings showed absence of cyto-albumin dissociation.

The patient was again reviewed by a neurologist and started on IV thiamine 200 mg thrice a day and injection methylcobalamin 100 μg once a week. There was a rapid improvement in cognitive functions of the patient, which prompted a diagnosis of WE. Thyroid function improved, and propylthiouracil was stopped in the second trimester. Even though her symptoms improved, there was residual motor weakness near term gestation with mild cognitive impairment. An elective cesarean section was planned at 37 weeks of gestation in view of the inability of the patient to participate in the course of normal vaginal delivery due to her residual lower limb weakness (bilateral lower limb motor power was 2/5 and upper limb motor power was 3/5) and high emotional lability. General anesthesia was the preferred anesthesia technique for this patient. A rapid sequence induction (RSI) and intubation was done. Injection rocuronium 60 mg (1.2 mg/kg) was used instead of succinylcholine, and nitrous oxide (N2O) use was avoided for maintenance of anesthesia. Routine minimum mandatory monitoring along with neuromuscular (NM) monitoring was done. The surgery lasted for 45 min and a healthy baby was delivered. The patient was successfully extubated with an uneventful postoperative stay. She was discharged 4 weeks later with mild cognitive impairment and improved motor power.

  Discussion Top

WE is an acute neuropsychiatric disorder resulting from thiamine deficiency characterized by the triad of encephalopathy, ophthalmoplegia, and ataxia.[2] Although commonly seen in alcoholics, a few cases (0.04%–0.13%) have been reported in nonalcoholics.[3] The risk of WE increases in HG due to poor intake, continued vomiting, increased thiamine requirement in pregnancy, and administration of dextrose-containing fluids.[3] The absence of the classic triad of WE in our case and the ascending symmetric polyneuropathy confused the diagnosis with GBS. MRI brain in WE shows hyperintensities in the thalamus and periaqueductal areas (93% specificity), but normal neuroimaging in our case further caused a delay in diagnosis.[4] A diagnosis of WE was made based on improvement in cognitive functions with IV thiamine. Determination of blood transketolase activity and thiamine pyrophosphate reflects the thiamine status in the body and can be done in such cases, but lack of its sensitivity and easy availability limits its usefulness in making the diagnosis.[4]

Transient thyrotoxicosis of hyperemesis gravidarum (TTHG) is a nonimmune hyperthyroidism of pregnancy reported in patients with HG.[5] As anti-TPO antibodies were negative and hyperthyroidism resolved in the second trimester with a resolution of hyperemesis in the present case, TTHG is a likely explanation for the deranged thyroid functions.

Critical care management of parturients with WE has been reported in the literature, but anesthetic management of these patients presenting for cesarean section is lacking. Neurological disease sequela such as persistent quadriparesis and cognitive impairment along with obstetric concerns makes them pose unique challenges to anesthesiologists. Routinely, neuraxial block is the preferred anesthesia for cesarean section because of its acknowledged benefits over general anesthesia. However, regional anesthesia in patients with preexisting neurological diseases has its own concerns. Upton and McComas have described “double-crush phenomenon,” which suggests that patients with preexisting neural compromise are more susceptible to injury at another site when exposed to a secondary insult which can be surgical or anesthesia-related factors.[6] This suggests that the theoretical risk of worsening of neurological disease with neuraxial block cannot be ignored in such patients in the postoperative period. Medicolegal concerns along with difficulty in the assessment of sensory motor blockade following neuraxial block are other major problems. Although the use of neuraxial block in parturients with neurological sequela has been reported in literature,[7] general anesthesia seems to be a safer option.[8] Use of succinylcholine should be avoided because of the increased risk of hyperkalemia in patients with prolonged immobilization.[7] Rocuronium is the preferred NM blocking drug for RSI in these patients. As our patient was on Vitamin B12 preoperatively, we avoided N2O for maintenance of anesthesia. Sanders reported a significant reduction (50%) in methionine synthase activity even after 45 min of N2O exposure.[9] To ensure favorable intubating condition, a higher dose of rocuronium was used. Upregulation of nicotinic receptors as a result of prolonged immobilization resulted in early NM blockade reversal (45–50 min) even with a higher dose of rocuronium (1.2 mg/kg).[10] NM monitoring should be done as a part of necessary monitoring in patients with coexisting neurological disorder undergoing general anesthesia.

Thus, to conclude, obstetric patients with preexisting neurological disease become a special subpopulation for anesthesiologists. A thorough knowledge of the current disease process, neurological sequela, and preoperative medications becomes important for a successful anesthetic management and safer maternal–fetal outcome. A higher risk of further neurologic damage with neuraxial anesthesia in patients who have an unstable or progressive neurologic disease makes the administration of general anesthesia a safer choice in these patients.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published, and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Goodwin TM. Hyperemesis gravidarum. Clin Obstet Gynecol 1998;41:597-605.  Back to cited text no. 1
Gascón-Bayarri J, Campdelacreu J, García-Carreira MC, Estela J, Martínez-Yélamos S, Palasí A, et al. Wernicke's encephalopathy in non-alcoholic patients: A series of 8 cases. Neurologia 2011;26:540-7.  Back to cited text no. 2
Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F. Hyperemesis gravidarum complicated by Wernicke encephalopathy: Background, case report, and review of the literature. Obstet Gynecol Surv 2006;61:255-68.  Back to cited text no. 3
Netravathi M, Sinha S, Taly AB, Bindu PS, Bharath RD. Hyperemesis-gravidarum-induced Wernicke's encephalopathy: Serial clinical, electrophysiological and MR imaging observations. J Neurol Sci 2009;284:214-6.  Back to cited text no. 4
Goldman AM, Mestman JH. Transient non-autoimmune hyperthyroidism of early pregnancy. J Thyroid Res 2011;2011.  Back to cited text no. 5
Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet 1973;2:359-62.  Back to cited text no. 6
Paul A, Bandyopadhyay KH, Patro V. Anesthetic management of a parturient with Guillain-Barre syndrome posted for emergency caesarian section. J Obstet Anaesth Crit Care 2012;2:40-3.  Back to cited text no. 7
  [Full text]  
Kopp SL, Jacob AK, Hebl JR. Regional anesthesia in patients with preexisting neurologic disease. Reg Anesth Pain Med 2015;40:467-78.  Back to cited text no. 8
Sanders RD, Weimann J, Maze M. Biologic effects of nitrous oxide: A mechanistic and toxicologic review. Anesthesiology 2008;109:707-22.  Back to cited text no. 9
Brull SJ, Meistelman C. Pharmacology of neuromuscular blocking drugs. In: Miller's Anesthesia. 9th ed.. Philadelphia, PA: Elsevier; 1910. p. 825-27.  Back to cited text no. 10


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