The present study compared the efficacy of two different doses of labetalol, for attenuation of hemodynamic response to laryngoscopy and intubation in hypertensive patients. Patients and methods: 75 hypertensive patients, aged 18-60 years undergoing elective surgical procedures, require general anesthesia and orotracheal intubation. Patients were allocated to any of the three groups (25 each), Group C (control) 5 ml 0.9% saline. Group L1 (labetalol) 0.15 mg/kg diluted with 0.9% saline to 5 ml. Group L2 (labetalol) 0.3 mg/kg diluted with 0.9% saline to 5 ml. In the control group 5 ml of 0.9% saline was given i.v. 5 min prior to intubation. In the L1 group 0.15 mg/kg of labetalol was given i.v. 5 min prior to intubation. In the L2 group 0.3 mg/ kg of labetalol was given i.v. 5 min prior to intubation. All the patients were subjected to the same standard anesthetic technique. Heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded prior to induction, at time of intubation and 1, 3, 5, and 10 min after intubation. Mean arterial pressure (MAP) and rate pressure product (RPP) were calculated. Results: Compared to placebo both the doses of labetalol (0.15 mg/kg) and (0.3 mg/kg) significantly attenuated the rise in heart rate, systolic blood pressure, and RPP during laryngoscopy and intubation. However, the difference was not statistically significant between both doses of labetalol at intubation, 1 min, 3 min and 10 min post-intubation. Conclusion: Both doses of labetalol (0.15 mg/kg and 0.3 mg/kg) attenuate hemodynamic response to laryngoscopy and intubation in dose dependent manner.

The present case highlights a rare occurrence of this tumor in the parotid gland, which until now was labeled as a tumor exclusive to minor salivary glands. Thus this entity should be kept as a differential while investigating mucinous tumors of parotid.

Freedom from pain has almost developed to be a fundamental human right. Providing pain relief via epidural catheters in thoracic and upper abdominal surgeries is widely accepted. Pain relief through this technique not only provides continuous analgesia but also reduces post-operative pulmonary complications and also hastens recovery. But being a blind procedure it is accompanied by certain complications. Hypotension, dura puncture, high epidural, total spinal, epidural haematoma, spinal cord injury and infection are some of the documented side effects of epidural block. There are case reports eliciting neurological complications, catheter site infections, paresthesias, radicular symptoms and worsening of previous neurological conditions. Few technical problems related to breakage of epidural catheter are also mentioned in the literature. The patient had no sequelae on long term follow up even when a portion of catheter was retained. We present a case report where epidural catheter punctured pleura in a patient undergoing thoracotomy for carcinoma oesophagus.

Vasoplegic syndrome (VPS) is defined as systemic hypotension due to profound vasodilatation and loss of systemic vascular resistance (SVR), despite normal or increased cardiac index (CI). It occurs in 9- 44% of cardiac surgery patients after cardiopulmonary bypass (CPB) and is associated with significant morbidity and mortality. The pathogenesis of VPS is multifactorial involving the activation of contact, coagulation, and complement systems and the activation of leukocytes. platelets and endothelial cells resulting in an imbalance in the regulation of the vascular tone; inducible nitric oxide synthase [iNOS] triggered by inflammatory cytokines during CPB produces nitric oxide (NO), which increases vascular levels of cyclic guanosine monophosphate (cGMP), resulting in vasodilation. leading to postcardiac surgery VPS. Standard treatment options for severe refractory VPS are extremely limited and include vasopressor support. latest Surviving Sepsis Campaign guidelines also consider that the best therapeutic management of vascular hypo- responsiveness to vasopressors could be a combination of multiple vasopressors, including norepinephrine (NE) and early prescription of vasopressin. This review will address the various definitions, risk factors, pathophysiology, potential cardiac candidates, and potential therapeutic interventions for VPS following cardiac surgery focussed on the outcome. This review did not require any ethical approval or consent from the patients.

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