Mridula Pawar

Patient-controlled analgesia with fentanyl for burn dressing changes.

In this randomized, double-blinded study in 60 ASA I or II adults with >20% body-surface area thermal burns, we investigated the feasibility of patient-controlled analgesia (PCA) with fentanyl for pain management during dressing changes and determined the optimal PCA-fentanyl demand dose. An initial loading dose of IV fentanyl 1 μg/kg was administered. Patients received on-demand analgesia with fentanyl (10, 20, 30, and 40 μg) whenever their visual analog scale (VAS) score was >2. Mean VAS scores in the 10 and 20 μg groups (7.73 ± 1.33 and 7.20 ± 1.21, respectively) were significantly higher than those in the 30 and 40 μg groups (4.47 ± 0.83 and 3.90 ± 0.63, respectively) (all P = 0.000). Demand/delivery ratios were significantly larger in the 10 and 20 μg groups (3.03 ±1.06 and 2.54 ± 0.49, respectively) than those in the 30 and 40 μg groups (1.36 ±0.34 and 1.37 ±0.36, respectively) (all P =0.000). VAS scores and demand/delivery ratios were comparable in the 30 and 40 μg groups (P = 0.260 and P = 0.977, respectively), which suggests comparable analgesic efficacy. There was no hemodynamic instability or respiratory depression. The optimal demand dose of PCA-fentanyl was 30 μg (5-min lockout interval) after an initial loading dose of IV fentanyl 1 μg/kg.

Neurotoxin envenomation mimicking brain death in a child: A case report and review of literature.

The spectrum of presentation of a victim of neurotoxic snake bite can range from mild ptosis to complete paralysis and ophthalmoplegia. We report a case of snake bite in a 10-year-old child who was comatosed with bilateral fixed dilated pupils and absent doll′s eye movement that was interpreted as brain death. Physicians need to be aware of the likelihood of snakebite presenting as locked in syndrome.

Comparison of priming versus slow injection for reducing etomidate-induced myoclonus: a randomized controlled study

Background Etomidate injection is often associated with myoclonus. Etomidate injection technique influences the incidence of myoclonus. This study was designed to clarify which of the two injection techniques—slow injection or priming with etomidate—is more effective in reducing myoclonus. Methods This prospective randomized controlled study was conducted on 189 surgical patients allocated to three study groups. Control group (Group C, n = 63) received 0.3 mg/kg etomidate (induction dose) over 20 s. Priming group (Group P, n = 63) received pretreatment with 0.03 mg/kg etomidate, followed after 1 min by an etomidate induction dose over 20 s. Slow injection group (Group S, n = 63) received etomidate (2 mg/ml) induction dose over 2 min. The patients were observed for occurrence and severity of myoclonus for 3 min from the start of injection of the induction dose. Results The incidence of myoclonus in Group P (38/63 [60.3%], 95% CI: 48.0–71.5) was significantly lower than in Group C (53/63 [84.1%], 95% CI: 72.9–91.3, P = 0.003) and Group S (49/63 [77.8%], 95% CI: 66.0–86.4, P = 0.034). Myoclonus of moderate or severe grade occurred in significantly more patients in Group C (68.3%) than in Group P (36.5%, P < 0.001) and Group S (50.8%, P = 0.046), but the difference between Groups P and S was not significant (P = 0.106). Conclusions Priming is more effective than slow injection in reducing the incidence of myoclonus, but their effects on the severity of myoclonus are comparable.

Green urine: A cause for concern?

128 Journal of Anaesthesiology Clinical Pharmacology | Volume 33 | Issue 1 | January-March 2017 with objects such as oral preoperative medication, prefilled epinephrine syringe, plastic wrapping from a filter, a heat and moisture exchanger, mucus, and an inferior turbinate, or herniation of the cuff have occurred but are all rare events.[5] This is an unusual case of ETT obstruction by tubercular granulation tissue, either an endobronchial focus or a tubercular lymph node eroding through the bronchus. However, in either case, this was asymptomatic and could not be picked up during preanesthetic evaluation. Lin et al. reported a case of acute ETT obstruction caused by unexpected hemoptysis in a patient undergoing surgery for Pott’s spine in prone position, which was relieved just by placing the patient supine (as happened in our case as well).[6] Further, FOB not only has a role in diagnosis of an adverse respiratory event in an intubated patient but also is a useful therapeutic tool as well.[5] An algorithm for the management of airway obstruction is to exclude ventilator, circuit, and ETT as causes step by step followed by considering and treating patient sources of resistance.[7]

Unilateral pulmonary edema during laparoscopic resection of adrenal tumor

Despite technological, therapeutic and diagnostic advancements, surgical intervention in pheochromocytoma may result in a life-threatening situation. We report a patient who developed unilateral pulmonary edema during laparoscopic resection of adrenal tumor.

Central anticholinergic syndrome in a neonate operated for tracheoesophageal fistula

Sir, n nSeveral drugs used in anaesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. We report a suspected case of central anticholinergic syndrome (CAS) in a neonate following general anaesthesia (GA) involving intra-operative use of anticholinergic agents. n nA one-day-old term male baby with tracheoesophageal fistula, weighing 2.5 kg, was posted for emergency surgical correction. Pre-operative examination revealed bilateral crepitations, oxygen saturation (SpO2) of 90% (room air) and heart rate (HR) of 150/min. Standard monitoring was established. Glycopyrrolate 12.5 μg and fentanyl 5 μg were administered intravenously (IV). Anaesthesia was induced with halothane in oxygen. The trachea was intubated with a tracheal tube of 3 mm ID under deep inhalational anaesthesia. Atracurium 1.25 mg IV was given, and respiration was controlled. A few minutes after intubation, before the patient was positioned for surgery, the baby developed bronchospasm, HR decreased to 40/min, and SpO2 was 70%. Atropine 0.1 mg IV and salbutamol inhalation were administerd via T piece, and ventilation continued with 100% oxygen. HR and SpO2 improved and surgery commenced after positioning. After few minutes, a similar episode occurred, and atropine 0.1 mg was repeated. During lung retraction, the patient again developed bradycardia and oxygen desaturation. Atropine 0.1 mg IV was administered as bradycardia persisted despite release of lung retraction and 100% oxygen administration. Surgery lasted for 1.5 h. At the end of surgery, after confirming adequate respiratory efforts, residual neuromuscular blockade was reversed with neostigmine 0.125 mg and glycopyrrolate 0.025 mg IV. n nEven though respiratory effort was adequate, the neonate was deeply sedated with no response to painful stimulation. He was normothermic, normoglycaemic with normal arterial blood gas parameters. Pupils were dilated bilaterally with poor reaction to light. The baby was suspected to have CAS. Due to non-availability of physostigmine, it could not be administered. The baby was not extubated and was maintained on T-piece with intermittent assistance of respiration. After 1 h, the baby started opening his eyes, moving his limbs and responding to touch with adequate respiratory efforts and thereafter his trachea was extubated. Pupils were mid-dilated with improved but sluggish response to light. Pupils returned to normal size 18 h post-operatively. The baby had an uneventful recovery. n nOur patient had delayed emergence from anaesthesia with bilateral dilated pupils. Common reasons for delayed emergence in a neonate include residual drug effect, hypoglycaemia, acid-base disturbances, hypoxia, hypercarbia and hypothermia.[1] The baby had none of these problems. Child had three episodes of desaturation with bradycardia. Bradycardia in a neonate is most commonly due to hypoxemia. Improvement in oxygenation improved desaturation, but bradycardia persisted, necessitating administration of atropine (0.1 mg) on each of the three occasions. A total dose of 0.3 mg of atropine (for bradycardia) and 25 μg of glycopyrrolate (intra-operatively) was administered. We used 0.1 mg of atropine because that is the minimum dose recommended in standard references.[2,3] Post-operatively, the baby was sedated with decreased responsiveness and bilateral dilated pupils. This suggests the possibility of CAS. Glycopyrrolate, even though a quaternary ammonium compound, can cause central effects in a neonate due to immature blood-brain barrier (BBB). n nIn CAS, excitation or depression symptoms can occur due to central nervous system effects of the acetylcholine (restlessness, agitation, hallucination, disorientation, convulsions, respiratory failure, coma).[4] Incidence of CAS is between 1% and 11.2% after GA.[5] CAS is well-defined in elderly adults, but it has been reported rarely in children and only a single case in neonate.[6,7] Kulka et al. reported that a 6-week-old infant had symptoms consistent with CAS following uneventful GA for hernia repair.[6] The child who had received 0.03 mg atropine responded to two doses of physostigmine, and he awoke spontaneously after 24 h.[6] Gillick reported a case in which partial reversal of central anticholinergic toxicity of atropine (0.09 mg/kg) by physostigmine resulted in an incipient muscarinic crisis in a neonate that was averted by glycopyrrolate.[7] Physostigmine, neostigmine or edrophonium may be administered as treatment. As neostigmine and edrophonium are quaternary amines, they cannot cross the BBB; they are used to treat peripheral effects of anticholinergic drug overdoses. Physostigmine, a tertiary amine, can cross the BBB and is used to treat the central effects of anticholinergic drug overdoses in dose of 0.03–0.04 mg/kg, repeated at 10–30 min intervals, if needed. n nCentral anticholinergic syndrome can develop in a neonate because of over dosage with atropine or glycopyrrolate. The use of atropine in 10–20 μg/kg dose (and not the minimum dose) could have averted this iatrogenic complication. The possibility of CAS should be considered in a patient with post-operative flushing, mydriasis, dry skin and mucous membranes, altered mental status or fever. Physostigmine, a tertiary amine, should be available in the operating room for treatment of CAS.

Massive hydrothorax following supracostal percutaneous nephrolithotomy

Sir, n nPercutaneous nephrolithotomy (PCNL) is used commonly for the treatment of large renal and upper ureteric calculi. We report a 30-year-old female who developed a massive hydrothorax diagnosed postoperatively following PCNL for left renal calculus. Standard anaesthesia with controlled ventilation was administered. PCNL was performed in the prone position with a left supracostal (between 11th and 12th rib) approach. Multiple attempts were required to reach the superior calyx. Intraoperatively the patient remained haemodynamically stable. The procedure lasted 120 min; blood loss was ≈ 400 mL. Following extubation the patient was comfortable and haemodynamically stable with oxygen saturation (SpO2) 98% on 40% oxygen. After 30 min, the patient complained of breathing difficulty. She was tachypnoeic, with SpO284% (O2 5 L/min). Air entry was absent in left hemithorax, with dullness on percussion. Chest radiograph revealed left hydrothorax [Figure 1a]. An intercostal chest drain with underwater seal was inserted in the left 5th intercostal space. Haemorrhagic fluid (850 mL) was drained. Patient experienced difficulty in breathing following rapid pleural decompression. Continuous positive airway pressure was given by face mask with 100% oxygen for 20 min. Thereafter, she was asymptomatic, SpO2 was 100% and arterial blood gas analysis was normal. Repeat chest radiograph 24 h later showed lung expansion [Figure 1b]. The drain was removed on the 3rd postoperative day. The patient was discharged on the 6th postoperative day. n n n nFigure 1 n nPostoperative chest radiograph showing (a) opacity of left hemithorax and (b) re-expansion of the lung at 24 h n n n nAnaesthetic challenges during PCNL include the potential for fluid absorption, dilutional anaemia, hypothermia, blood loss, injury to adjacent organs and pleural space violation.[1,2] The renal calyceal system can be accessed via a subcostal or supracostal route. The supracostal access (above the 12th or 11th rib) is commonly used as it provides direct access to the upper, middle and lower calyx and the upper ureter.[2] However, this approach can potentially damage the lung and pleura resulting in hydrothorax, pneumothorax or hydropneumothorax.[1] n nPleural injury can be avoided by supracostal puncture over the most lateral portion of the 12th rib as this portion of the diaphragm is not covered by a pleural reflection.[3] The intercostal puncture is made in the lower half of the intercostal space to avoid injury to intercostal vessels.[4] The supracostal approach requires coordination with the anaesthesiologist to control ventilation. The needle is passed through the retro-peritoneum and diaphragm during complete exhalation to prevent injury to the lung. The passage of the needle through the renal parenchyma to the collecting system is done during deep inspiration (the kidney gets displaced downwards). An Amplatz sheath is used to maintain low-pressure irrigation that can reduce the risk of pleural effusion and extravasation.[4] n nReasons for development of hydrothorax are three-fold: (a) Inadvertent entry into the pleura; (b) inadequate tamponade of the nephrostomy tract combined with inadequate drainage of the kidney after the puncture; and (c) failure to seal the tract with a working sheath during stone removal.[5] n nHydrothorax and pneumothorax can be difficult to identify during PCNL. Intraoperatively, a decrease in SpO2 and a significant increase of airway pressure is suggestive of hydrothorax. The diagnosis can be confirmed with a chest radiograph; with the patient in the prone position, fluid can be seen tracking along the lateral borders of the chest cavity and compressing the ipsilateral lung.[3] In the immediate postoperative period, pleural injury presents clinically with poor SpO2, dyspnoea and tachypnoea.[4] A postoperative chest X-ray is mandatory. The treatment of hydrothorax depends on patient symptoms and its extent.[4] Patients with no or mild symptoms and minimal effusion are managed conservatively; those with significant symptoms and large pleural effusion need intercostal drainage. n nRe-expansion pulmonary oedema, an uncommon complication following drainage of a pneumothorax or pleural effusion, presents clinically as cough, chest discomfort and hypoxemia. Risk factors include young age, long duration of lung collapse and rapid re-expansion. Treatment is largely supportive (oxygen supplementation, noninvasive and invasive ventilation). n nA high index of suspicion should be maintained when PCNL is performed with a prolonged operating time, multiple tracts and supracostal access. The access puncture should be performed in complete lung deflation and ventilator stand-still in coordination with the anaesthesiologist to minimise the risk of pleural injury. A chest X-ray should be performed promptly in symptomatic postoperative patients to exclude intrathoracic injury. Hydrothorax, haemothorax and/or pneumothorax sustained during PCNL may necessitate chest tube placement.