Chapter 05

Disulfiram Like Reaction

Dr. Vasanthi Vidyasagaran*

Department of Anaesthesiology, Kauvery Hospital, Chennai, Tamilnadu, India



A 29-year-old woman, near term, was admitted to the obstetric unit with complaint of inability to feel foetal movements. There was no significant antenatal history except mild fever for the past 2 days. She had severe malaise and loss of appetite. CTG confirmed foetal compromise and she was to be taken up for an emergency LSCS.

On examination, chest was clear and BP = 110/70 mm Hg, PR = 100 beats/min. She was anxious and her temperature 99°F. Her blood investigations showed Hb = 10 g/dl, WBC = 15000, and platelets = 100000. Renal functions were normal. Blood culture and urine culture samples were sent.

Caesarean section was planned under spinal anaesthesia as the patient had a meal just one hour ago. Spinal anaesthesia was administered in the sitting position in L2-L3 space with 2 ml 0.5% Bupivacaine. The intraoperative period was quite uneventful except for a single reading of BP 86/48 mm Hg when the baby was delivered. It picked up to 100/60 mm Hg within 5 min and the pulse rate went up to 120/min even without administering any vasopressors. Oxygen saturation was 96-98% throughout.

At this point, her temperature went up to 1000 for which 1g Paracetamol was given. Surgery was completed in half an hour and she was shifted to the postoperative ward. The next day she complained of weakness in both her lower limbs and was unable to stand or walk.

She was still febrile, with temperature of 101°F. Lungs were clear and chest x-ray was normal. She was given IV antibiotics, Paracetamol and steroid. By evening, she complained of numbness ascending above her umbilicus along with difficulty in breathing. Suspecting viral fever, supportive therapy was continued and a physician opinion was sought.

A complete panel of blood investigations were sent for. Lumbar puncture was done and CSF sent for analysis. Typical albuminocytological dissociation (elevated CSF protein with normal CSF cell count) on the CSF sample clinched the diagnosis of Guillain Barre Syndrome. Patient was intubated, and given ventilatory support, and IV Immunoglobulin was administered. She responded well, and extubated in 2 days. She did not require any further treatment like plasmapheresis. Both mother and baby were discharged after 10 days.


GA vs spinal: Spinal anaesthesia was administered as it is common practice for LSCS and the patient had low grade fever. There was no contraindication for spinal and in fact it seemed quite appropriate since it was a patient with full stomach, having had a meal just one hour prior to the procedure. If the patient had any neurological symptoms before surgery, general anaesthesia would have been the choice as neuraxial anaesthesia may trigger or aggravate disease process.

Differential diagnosis of fever with malaise:

Viral and Bacterial infections affecting both the mother and foetus. There could be systemic illness like appendicitis or urinary tract infections or even serious conditions like pneumonia and meningitis.

Differential diagnosis of post-partum weakness of legs;

Acute myelopathy, polyneuropathy, HIV peripheral neuropathy, hysterical paralysis, paraneoplastic neuropathy, spinal cord syndromes, and spinal anaesthesia related neurological injury.

Guillain-Barre Syndrome (GBS) is an acute demyelinating polyneuropathy, characterized by progressive, ascending paralysis and areflexia, with or without abnormal sensory function. About one-third of the patients with GBS will require mechanical ventilation and most GBS-related deaths occur as a result of respiratory failure. Many clinical variants have been documented in literature.

Most patients complain of paraesthesia or numbness beginning in the toes and finger tips and progressing upwards. Autonomic changes may be tachycardia or bradycardia paroxysmal hypertension and orthostatic hypotension and urinary retention. The respiratory complaint include difficulty in breathing and swallowing.

GBS is a rare complication in the peripartum period, and if it occurs, can get precipitated in the post- partum period. Pregnancy is associated with a decrease in cellular immunity and increase in humoral immunity – this shift is because of production of Interleukin 10. After pregnancy is terminated, this is reversed and accounts for the increased incidence and worsening of symptoms in the post-partum period.

Obstetricians, anaesthetists and critical care physicians must be aware of the risks of relapsing GBS in the immediate postpartum period. Surgery and anaesthesia may be triggers for relapse in association with an overall increase in pro-inflammatory cytokines in the postpartum period.

Immunomodulation with plasma exchange and IV IG have been found to improve treatment outcomes. 70-80% of patients recover fully. Physical occupational and speech therapy may be required for an overall improvement of a patient.

Our case was unique as the lady responded well to IV IG, and did not require mechanical ventilation for long periods. She made a good recovery. Timely appropriate intervention and management saved our patient.


  1. D.H. Chestnut, L.S. Polley, L.C. Tsen, et al. Chestnut’s obstetric anesthesia: principles and practice. (4th Ed.) Elsevier, Philadelphia (2009), p. 1066
  2. A.K. Jacob, S.L. Kopp Regional anesthesia in the patient with pre-existing neurologic disorders. Adv Anesth, 29 (2011), pp. 1-18
  3. S Meenakshi-Sundaram1, K Swaminathan2, SN Karthik1, S Bharathi1 Relapsing Guillain-Barre syndrome in pregnancy and postpartum Annals of Indian Academy of Neurology 2014 Volume : 17 Issue : 3 Page : 352-354
  4. Brooks H, Christian AS, May AE. Pregnancy, anaesthesia and Guillain Barré syndrome. Anaesthesia 2000; 55:894-8.
  5. Steiner I, Argov Z, Cahan C, and Abramsky O. Guillain-Barré syndrome after epidural anesthesia: Direct nerve root damage may trigger disease. Neurology 1985;35:1473-5
  6. A good physical and mental health is the best wealth for any human being.


Chapter 06

Hypokalaemia with Laxative Abuse

An 80-year-old man weighing 60 kg was posted for inguinal hernia repair. History did not reveal any major medical or surgical illness, or drug intake for the same. His preoperative investigations were within normal limits for his age. Hb = 10.2, PCV 35, ECG – T wave inversion in V1 and V2, urea =34mgs. creatinine=1.1, chest x-ray – normal. No further investigations were done as he had no signs and symptoms of any systemic illness.

He was preloaded with 500 ml of crystalloids and a subarachnoid block was given with patient in right lateral position using a 25G Quincke needle in the L3-L4 space. 3 ml of 0.5 % Bupivacaine was injected. HR was maintained at 65 beats/minute and BP around 100/60 mm Hg. There was one incident of a drop- in pressure to 80/50 which was treated with 3 mg of Ephedrine. As the surgery proceeded he complained of increasing tiredness, weakness and discomfort. There was no further alteration in haemodynamics. Bedside glucose level was checked and it was within normal limits.

The ECG gradually started showing deepening of T wave inversions and U waves. Confirmation with a 12 lead ECG also showed the presence of U waves. We sent his blood sample for sugar and electrolytes. His serum potassium turned out to be 2.5 meq/L! We commenced slow potassium correction, and once the procedure was over he was shifted to the ICU where further correction of the potassium level was done, with continuous ECG monitoring. He recovered well and did not suffer any post-operative complication.

On probing into history, he said that he suffered from constipation and was taking laxatives for the past 20 years.


Patients do not often reveal the history of taking some drugs like herbal medicines, vitamins, and laxatives. They feel it is unnecessary rather unimportant. We must probe into the history. In patients, particularly in the elderly, on diuretics and laxatives preoperative check on sodium and potassium levels is important.

Prolonged hypokalaemia from chronic laxative abuse is recognized as the cause of chronic tubule- interstitial disease, known as ‘hypokalaemia nephropathy’, but it is not clear whether it contributes to acute kidney injury (AKI). Hypokalaemia from eating

disorders affects renin angiotensin system and predisposes to renal impairment. Chronic potassium depletion could lead to irreversible damage to the renal tubule.

Types of laxatives

  1. Bulk forming: Fibrecon, Methyl cellulose, Wheat dextrin
  2. Stool softeners: Docusate
  3. Lubricants: Mineral oil
  4. Stimulants: Dulcolax, Senokot, Castor oil (may be used in irritable bowel; colon becomes cathartic on regular use)
  5. Hyperosmotic: Saline laxatives (like Milk of Magnesia, Sulphate salts, Citrate salts), Lactulose, Glycerine suppositories – They must not be used on regular basis; cause fluid and electrolyte depletion and affect renin angiotensin system

Potassium correction

  • For every 1 mEq/L decrease in serum potassium, the potassium deficit is approximately 200-400 mEq
  • Mild or moderate hypokalaemia (potassium level of 2.5-3.5 mEq/L) are usually asymptomatic; if these patients have minor symptoms, they may need only oral potassium replacement therapy
  • If cardiac arrhythmias or significant symptoms are present, aggressive therapy must be initiated
  • If the potassium level is less than 2.5 mEq/L, intravenous potassium should be given with continuous ECG monitoring, and check serial potassium levels
  • The serum potassium level is difficult to replenish if the serum magnesium level is also low. Look to replace both.
  • Oral potassium is absorbed readily but may not be tolerated well
  • Intravenous potassium: highly irritating to veins, can be given only in relatively small doses, generally 10 mEq/h. Under close cardiac supervision in emergent circumstances, 40 mEq/h can be administered through a central line
  • Oral and parenteral potassium can safely be used simultaneously
  • Practical purposes: 10 ml 7.46% Potassium ampoule approximately equates to 0.746 g Potassium (elemental). 40 meq = 1600 mg elemental Potassium. Hence diluting 2 ampoules of 10% Potassium chloride in 100 ml 0.9% Normal Saline bag and administering through a central line over one hour may help emergent correction.


  1. Eun-Young L, et al. Does hypokalaemia contribute to acute kidney injury in chronic laxative abuse? Kidney Res Clin Pract 2015;34(2):109-112.
  2. Fleischer N, et al. Chronic laxative-induced hyperaldosteronism and hypokalaemia simulating Bartter’s syndrome. Ann Intern Med. 1969;70(4):791-8.
  3. Fleming BJ, et al. Laxative-induced hypokalaemia, sodium depletion and hyperreninemia. Effects of potassium and sodium replacement on the renin-angiotensin-aldosterone system. Ann Intern Med. 1975;83(1):60-2.
  4. Seguro AC, et al. Effect of potassium depletion on ischemic renal failure. Nephron, 1989;51:350-354.
  5. Greenlee M, et al. Narrative review: evolving concepts in potassium homeostasis and hypokalaemia. Ann Intern Med. 2009;150:619-625.