Could postoperative pulmonary oedema be attributed to the use of neostigmine?

1. Raiger LK, Naithani U, Vijay BS, Gupta P, Bhargava V. Noncardiogenic pulmonary oedema after neostigmine for reversal: A report of two cases. Indian J Anaesth 2010;54:338-41. 2. Oswalt CE, Gates GA, Homstrom MG. Pulmonary edema as a complication of acute airway obstruction. JAMA 1977;238:1833-5. 3. Fremont RD, Kallet RH, Matthay MA, Ware LB. Postobstructive pulmonary edema: A case for hydrostatic mechanisms. Chest 2007;131:1742-6. 4. Kallet RH, Daniel BM, Gropper M, Mathay MA. Acute pulmonary edema following upper airway obstruction: Case reports and brief review. Respir Care 1998;43:476-80. 5. Reed CR, Glauser FL. Drug-induced noncardiogenic pulmonary edema. Chest 1991;100:1120-4. Could postoperative pulmonary oedema be attributed to the use of neostigmine?

Sir, I read with interest the case report by Raiger et al, [1] titled "Non-cardiogenic pulmonary oedema after neostigmine for reversal: A report of two cases." The authors had described two cases of pulmonary oedema after routine surgeries. One patient developed it after tracheal extubation and required a very short period of mechanical ventilation. A laryngeal pack was used in this patient. The other patient developed it before tracheal extubation and required a relatively longer period of mechanical ventilation. This patient was reported to have difficulty in breathing and hence tracheal extubation was delayed.
Post-obstructive pulmonary oedema is caused by significant fluid shifts resulting from changes in intrathoracic pressure. [2] Negative intrathoracic pressure generated, when a patient attempts to inspire against a closed glottis or obstructed airway, leads to increase in venous return and a consequent rise in pulmonary venous pressure. This leads to a hydrostatic gradient with fluid moving from high pressure (pulmonary venous system) to low pressure (pulmonary interstitium and airspaces). [3] The negative intrathoracic pressure, along with the resultant hypoxia, also depresses the cardiac output by increasing myocardial wall stress and systemic vascular resistance, which increases the pulmonary venous pressure further. [4] Laryngospasm has been reported to be the cause in >50% of cases, whilst other causes include tracheal secretions, hiccups, and biting the endotracheal tube.
Drug-induced non-cardiogenic pulmonary oedema may be due to a pulmonary venoconstriction, capillary leak syndrome, intravascular fluid volume overload, and/or reduced serum oncotic pressure. [5] Drugs known to cause the above have been enumerated by Reed and Severe pain and hypertension following intravesical instillation of formalin necessitating epidural analgesia DOI: 10.4103/0019-5049.72660

Sir,
A 75-year-old, American Society of Anesthesiology Grade II male patient, a known case of carcinoma of the urinary bladder, who had previously undergone transurethral resection of the bladder tumour, received intravesical BCG and six cycles of radiotherapy, was referred to our hospital with persistent hematuria for seven months. A diagnosis of post-radiotherapy haemorrhagic cystitis was made. The patient twice underwent cystoscopy with clot evacuation for the same under subarachnoid block. However, the hematuria persisted, necessitating repeated transfusions of packed Red Blood Cells. As a last-ditch effort to stop the diffuse bleeding, an old technique of intravesical instillation and irrigation with formalin was planned. [1] The patient was a diabetic on insulin. He had no other comorbid disease. His preoperative haemoglobin was 7.4 g% and coagulation profile was within normal limits.
In the view of the short duration of the procedure, general anaesthesia was planned. Following intravenous fentanyl (60 µg) and propofol (100 mg), a Pro-seal laryngeal mask airway was inserted. Anaesthesia was maintained with O 2 , N 2 O, isoflurane. The patient was placed in lithotomy position and 4% formalin was instilled intravesically. Formalin was kept in situ for 20 min, after which the bladder was evacuated. There was an immediate hypertensive response following formalin instillation, the blood pressure rose from a baseline value of 110/80 mmHg to 190-180/120-100 mmHg with a pulse rate of 86 beats/min. The hypertensive response persisted despite repeating fentanyl (90 µg). After the procedure, on awakening, the patient complained of severe, unbearable pain in the suprapubic region despite repeated doses of IV fentanyl and morphine. His blood pressure continued to remain high. To alleviate his pain an epidural catheter was inserted in the L2-3 space and 10 ml of 0.125% bupivacaine administered. After 20 min the pain subsided and his vitals returned to normal.
Formalin has a dessicating effect when applied to living tissue; it hydrolyzes proteins and coagulates superficial tissue. This effect controls the haemorrhage from telangiectatic capillaries in the mucosal and submucosal layers. [1] Sloughing of the urothelium, local oedema and inflammation cause severe pain. Regeneration can take up to three weeks. Suprapubic pain, dysuria, a reduction in bladder capacity, urgency and incontinence are known complications. [1] The severity of the pain requires that, where possible, the procedure should be carried out under regional anaesthesia. Not many anaesthesiologists may be aware of the severe pain engendered by the intravesical instillation of formalin and we wanted to share our experience. We came across only one other report where suprapubic pain following formalin instillation was managed with intravesical lidocaine. [2] However, the duration of pain relief with such a technique would be limited. An epidural catheter offers the advantage of repeated dosing which can be beneficial, as our patient needed epidural morphine for two days.

Anjolie Chhabra, Krithika Krishnan
Department of Anaesthesiology and Intensive Care, All India Institute of Medical Sciences (AIIMS), New Delhi, India