INTRA-OPERATIVE

Chapter 13

Halothane and Adrenalin: A Deadly Combination

Carotid blowout

Dr. Vasanthi Vidyasagaran*

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

*Correspondence: Vasanthi.vidyasagaran@gmail.com

Dr. Vasanthy Vidyasagaran Muralidharan

A 19-year-old girl weighing 51 kg was posted for FESS with septoplasty. On examination, her pulse rate was 98/min, BP was 110/70, and no abnormality was detected on examination of cardiac and respiratory systems. She was an ASA 1 patient. After antibiotic administration and aspiration prophylaxis she was taken up for surgery under GA.

She was pre-oxygenated with 100% oxygen. General anaesthesia was induced with Propofol 100 mg, Fentanyl 60 mcg, and trachea intubated with size 7 cuffed oral ETT. Atracurium 25 mg was used as muscle relaxant. For maintenance 35:65 mixture of O2:N20 was used; Halothane 1-2% was used for anaesthesia and for control of blood pressure which was maintained at 90/60 mm Hg with MAP around 65 to 70 mm of Hg.

The first 45 minutes were uneventful. The ENT surgeons then infiltrated the nasal septum with premixed 2% lignocaine and adrenaline. Soon after, the patient developed tachycardia, drop in blood pressure followed by loss of capnography trace and desaturation. Patient became pulseless. The BP was not recordable, ECG showed ventricular tachycardia.

Cardiac arrest with VT was recognised and immediate CPR commenced. Defibrillator trolley was moved and patient was defibrillated with 200J. The rhythm reverted to normal after two shocks. She was started on Amiodarone 50 mg slow bolus and continued as an infusion. Surgery was quickly completed and she was shifted to ICU for further management. She recovered well with no further sequelae.

Discussion

Interaction between Halothane and Adrenaline is dangerous and can have serious consequences. Though halothane is not frequently used in recent times, it is still being used in some centres in India. Newer inhalational anaesthetic may also trigger arrhythmias.

Ventricular tachycardia (VT) will be associated with hypotension, and possible loss of cardiac output. ECG monitoring is essential for diagnosing VT, (which again is not being done routinely in some centres in spite of repeated, frequent instructions and reminders) ACLS protocols must be immediately followed.

Communication between surgeon and the anaesthesiologist plays a vital role in the OR. The surgeon could have warned about the use of lignocaine with adrenaline in the septum. The anaesthesiologist should have been vigilant and must have discontinued Halothane before infiltration. This clinical picture could also have also been due to injecting lignocaine with adrenalin into a vessel since, aspiration before infiltration is often ignored by the surgeon and the nasal septum is an area where absorption of the drug is high and extreme caution must be exercised while infiltrating local anaesthetic with Adrenalin.

Several studies have identified disruptive behaviour among doctors who do not adhere to norms and theatre discipline, endangering the life of the patient. This has been found to be more common among surgeons and there should be a system to monitor and control such behaviour to ensure patient safety.

Safer drugs like Dexmedetomidine are available for hypotensive anaesthesia; Halothane may not be the right choice. It is also advisable to play safe, not overdoing hypotension. Many patients who come up for sinus surgery have reactive airway and asthma. They are usually on beta agonists like Salbutamol and Deriphylline. When Lignocaine with Adrenaline is infiltrated, tachycardia and undue hypertension may be precipitated. This surgery usually requires a good surgical field and hypotensive anaesthesia is desired. infiltration alone may not produce the desired effect. The anaesthetist may need to use antihypertensive drugs to control the blood pressure.

The hallmark of a good anaesthetic technique is good ventilation, and prevention of wide fluctuations in haemodynamics. When both are well maintained, the intraoperative course is usually very smooth, and recovery is excellent.

Lignocaine has been used as a treatment of ventricular tachycardia. But when the VT is caused due to Lignocaine itself, Amiodarone is the drug of choice. In general, Amiodarone has replaced Lignocaine as the first line drug for ventricular arrhythmias.

Recognition of shockable rhythm and early defibrillation is essential in cardiac arrest situation to expect good recovery. Presence of automated electrical defibrillators in hospitals is useful as it guides juniors and paramedical staff in such situation.

References

  1. Maynard B. Chenoweth. Modern Inhalational anaesthetics. 2012;193.
  2. Gallager JD, et al The effects of Halothane on Ventricular tachycardia in intact dogs. Anaesthesiology 1991;75:866-875.
  3. Miller RA, et al. Ventricular tachycardia during halothane anaesthesia. Anaesthesia 1958;13:2
  4. Ventricular tachycardia during general anesthesia in a patient with … https://www.ncbi.nlm.nih.gov/pubmed/12670819
  5. Ventricular tachycardia during general anesthesia in a patient with … fentanyl and rocuronium, and initially maintained with nitrous oxide and halothane. After 20 …PDF] peri-operative cardiac arrhythmias: part two ventricular … – aagbi https://www.aagbi.org/…/285%20Perioperative%20Cardiac%20Dysrhythmias%20-%2…May 6, 2013 – ATOTW 285 – Perioperative cardiac dysrhythmias – Part 2, Ventricular dysrhythmias.

Chapter 14

Hypoglycaemia in an Alcoholic

A 40-year-old man was admitted to the emergency following a road traffic accident. He was diagnosed to have a compound fracture of his left tibia and fibula. He was in severe pain. The orthopaedic surgeon wanted to take up the case immediately to prevent complication like sepsis and loss of a limb.

On examination, patient was conscious but under the influence of alcohol. His PR was 118/min, blood pressure was 140/80. Chest examination did not reveal anything significant. As it was being taken up as an emergency, only his haemoglobin and urine analysis were done, and found to be normal. A Ringer Lactate drip was started and he was taken up under combined epi spinal anaesthesia.

A needle within needle technique was used in the L2-L3 space. 3cc of 0.5% Bupivacaine, with Fentanyl 50 mcg was given intrathecally. The epidural catheter was placed with tip at LI, but was not activated. Patient was hemodynamically stable and the surgery started. During the procedure of reaming the tibia for intramedullary nailing, he slowly became drowsy and unresponsive. His BP dropped to 90/50 mm Hg, PR was 120/min and the ECG showed sinus tachycardia. 6 mg Ephedrine was given assuming spinal hypotension.

The pressure picked to 110/70, pulse rate increased further to 130/min, he continued to remain unconscious. Securing the airway with endotracheal tube was contemplated, but his oxygenation was maintained and respiratory effort was good. The cause of his reduced level of consciousness was a puzzle.

Differential diagnosis of reduced level of consciousness included alcohol intoxication, total spinal, hypoglycaemia, fat embolism and air embolism. His ECG was normal and respiration was not affected. Blood glucose level was done. CBG value was 48 g/dl. The cause for loss of consciousness was diagnosed to be hypoglycaemia. Following administration of 50 ml of 25 percent dextrose he rapidly regained consciousness.

Discussion

A total spinal was excluded because his breathing was unaffected and hypotension responded to Ephedrine. Saturation was maintained at 96%, hence, a diagnosis of embolism was ruled out. Blood gas results showed no hypoxia. Since there was a positive finding of hypoglycaemia, and he regained consciousness after administering Dextrose, it was concluded to be a case of hypoglycaemia.

Patients consuming alcohol are prone for hypoglycaemia especially after a prolonged fasting period. Metabolism of alcohol in the liver is by oxidation. This prevents the substrates required for gluconeogenesis (lactate, alanine) from being utilised. Glycogen stores are depleted, and intestinal absorption of glucose is absent.

Cognitive dysfunction and restlessness is the first sign of hypoglycaemia. Anaesthesia may mask cognitive dysfunction and hence anaesthesiologists should measure blood glucose levels in starved patients with a history of significant alcohol intake. In this case, clear history was not available due to emergency nature of surgery, which is not uncommon. Serum glucose level is the single most important test in this context.

Serum electrolyte levels including bicarbonate must be done in patients under influence of alcohol to identify alcohol induced ketoacidosis. Measuring serum ethanol level is controversial as it is unlikely to affect the management. Similar scenario can happen in diabetics as well as non-diabetics. Ethanol affects central nervous system by various mechanisms – directly acting on NMDA receptors, or indirectly as effects of hypoglycaemia. Ethanol inhibits gluconeogenesis (patients with less glycogen stores more affected).

Alcohol is metabolised in liver, gets broken down by alcohol dehydrogenase (ADH). It is further broken down by aldehyde dehydrogenase. This reaction utilises enzymes Nicotinamide Adenine Dehydrogenase (NAD) and Cytochrome P450. In the process, alcohol alters the ratio NAD: NADH, slows down neoglucogenesis and causes accumulation of beta hydroxy butyric acid. Vomiting and volume depletion in alcohol intoxicated patients aggravate the situation. Hypoglycaemia is a life-threatening complication if left untreated, causing loss of consciousness, arrhythmias, shock, delirium tremens, or even a cardiac arrest. Hence suspicion of hypoglycaemia and immediate treatment in the perioperative period, especially for patients under the influence of alcohol is crucial.

References

  1. Huang Z, Sjoholm A. ‘Ethanol acutely stimulates islet blood flow, amplifies insulin secretion and induces hypoglycaemia via NO and vagally mediated mechanism’. Endocrinology 2008;149:232-6.
  2. Brent J. Fomepizole for ethylene glycol and methanol poisoning. N Engl J Med. 2009;360(21):2216-23.
  3. Kraut JA, Kurtz I. Toxic alcohol ingestions: clinical features, diagnosis, and management. Clin J Am Soc Nephrol. 2008;3(1):208-25.

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