Ghansham Biyani

Comparison of performance and efficacy of air-Q intubating laryngeal airway and flexible laryngeal mask airway in anesthetized and paralyzed infants and children.

Flexible laryngeal mask airway is a commonly used supraglotic airway device (SAD) during ophthalmic surgeries. Air‐Q intubating laryngeal airway (ILA) is a newer SAD used as primary airway device and as a conduit for intubation as well. Available literature shows that air‐Q performs equal or better than other SADs in children and adults. However, limited data is available using air‐Q in infants and small children <10 kg. So, our aim was ‘To compare the performance and efficacy of these two devices in infants and small children’. Our hypothesis is that air‐Q due to its improved cuff design will yield better airway seal pressures and improved laryngeal alignment as compared to flexible laryngeal mask airway.

Middle East respiratory syndrome: A new global threat

The outbreak of Middle East respiratory syndrome (MERS) is reported from Saudi Arabia and the Republic of Korea. It is a respiratory disease caused by coronavirus. Camels are considered as a source for MERS transmission in humans, although the exact source is unknown. Human-to-human transmission is reported in the community with droplet and contact spread being the possible modes. Most patients without any underlying diseases remain asymptomatic or develop mild clinical disease, but some patients require critical care for mechanical ventilation, dialysis and other organ support. MERS is a disease with pandemic potential and awareness, and surveillance can prevent such further outbreaks.

Acute respiratory failure and mechanical ventilation in pregnant patient: A narrative review of literature.

Physiological changes of pregnancy imposes higher risk of acute respiratory failure (ARF) with even a slight insult and remains an important cause of maternal and fetal morbidity and mortality. Although pregnant women have different respiratory physiology and different causes of ARF, guidelines specific to ventilatory settings, goals of oxygenation and weaning process could not be framed due to lack of large-scale randomized controlled trials. During the 2009 H1N1 pandemic, pregnant women had higher morbidity and mortality compared to nonpregnant women. During this period, alternative strategies of ventilation such as high-frequency oscillatory ventilation, inhalational of nitric oxide, prone positioning, and extra corporeal membrane oxygenation were increasingly used as a desperate measure to rescue pregnant patients with severe hypoxemia who were not improving with conventional mechanical ventilation. This article highlights the causes of ARF and recent advances in invasive, noninvasive and alternative strategies of ventilation used during pregnancy.

Airway management in a patient with blunt trauma neck: A concern for anesthesiologist

Abstract Laryngo-tracheal injuries resulting from blunt trauma neck are fortunately rare, but may have dire consequences. A high index of suspicion is required to make the diagnosis. Here we report a case of airway management of a patient with blunt trauma neck with tracheal tear posted for tracheal tear repair under GA. Tracheostomy, FOB guided intubation and direct laryngoscopy are the standard methods used to secure the airway in these patients, but sometimes they may aggravate the underlying injury. Technique of choice depends upon patient’s condition, urgency, and experience of anesthesiologist and surgeon.

Sedation in a child with Klippel-Feil syndrome scheduled for magnetic resonance imaging

imaging (MRI) suites to perform imaging in children and uncooperative adults. The choice of anesthesia may range from moderate sedation to general anesthesia depending on the patient’s characteristics and/or institutional protocols. Due to challenges in accessing patients in the MRI suite, the anesthetic technique should be chosen carefully. This is even more important when the patient has an anticipated difficult airway. A four-year-old male child weighing 14 kg presented with delayed developmental milestones, diminished hearing, and no organized speech. The patient had a diagnosis of Klippel-Feil syndrome (KFS). Ultrasonography of the abdomen and echocardiography ruled out any associated systemic defects and the patient was scheduled for MRI of the brain and cervical spine for further evaluation. After a failed attempt at sedating the patient with oral chloral hydrate in the MRI suite, he was scheduled for MRI under general anesthesia. The pre-anesthetic evaluation showed that the patient had a short webbed neck with limited extension and a low posterior hairline (Fig. 1). Due to an anticipated difficult airway and the diagnostic nature of the procedure, we planned to provide sedation with dexmedetomidine via a backup laryngeal mask airway if required. Intravenous access was obtained with a 22-gauge cannula after application of a eutectic mixture of local anesthetics. Baseline vitals (electrocardiography [ECG], blood pressure, and pulse oxygen saturation [SpO2]) were recorded. A loading dose of 1 μg/kg dexmedetomidine was administered over 10 minutes followed by an infusion of 0.7 μg/kg/h dexmedetomidine. Monitoring of the depth of sedation was performed based on the Ramsay Sedation Score and the patient was moved onto the MRI table once a score of 5 was achieved; following this, ear plugs were applied. Oxygen supplementation was achieved with fraction of inspired oxygen of 0.28 with continuous monitoring of ECG, noninvasive blood pressure, SpO2, and end-tidal carbon dioxide throughout the diagnostic procedure, which lasted approximately 50 minutes. All of the above parameters were within normal limits and no additional intervention was required. At the end of the procedure, dexmedetomidine infusion was stopped and the patient was responsive to verbal stimuli after 7 minutes. The patient was discharged home once the discharge criteria were met. KFS is an inherited condition with the classic triad of a short webbed neck, limited neck movements, and a low posterior hairline [1,2]. KFS may be associated with conductive or sensorineural deafness, congenital heart disease (most commonly a ventricular septal defect), cleft palate, rib defects, and scoliosis. Anesthetic challenges include a difficult airway, cervical spine instability, and associated cardiovascular and genitourinary system abnormalities. There is an increased risk of spinal cord injury during maneuvers such as laryngoscopy, intubation, and placing the patient in an appropriate position for the procedure [3]. Patients with KFS may need to be anesthetized for diagnostic procedures, surgical correction of congenital defects, or any othLetter to the Editor

Anesthetic management of a child with autistic spectrum disorder and homocysteinemia

Autistic spectrum disorder (ASD) is a developmental disability of the central nervous system with rapid worsening. A subset of patients also has mitochondrial dysfunction leading to increased sensitivity to various anesthetic agents. Rarely, gene mutation in these patients results in homocysteinemia which causes higher incidences of thromboembolism, hypoglycemia, and seizures. Anesthetic management of ASD with homocysteinemia and refractory seizures has not been previously reported.

“Zero” diastolic blood pressure

A 40-year-old male patient with normal hemodynamics got admitted to our Intensive Care Unit (ICU) for postoperative observation. Multipara monitor was attached. It displayed noninvasive blood pressure (NIBP) of 130/0 mmHg [Figure-1]. On repeated measurements, diastolic blood pressure (DBP) was always reported to be zero while patient’s systolic blood pressure (SBP) varied between 130 and 180 mmHg. NIBP was measured in the opposite arm which also showed zero DBP. On auscultatory measurement using mercury sphygmomanometer, patient’s blood pressure (BP) was 140/70 mmHg. Similar values were recorded when a new multipara monitor was attached. This faulty monitor was attached to another patient and it displayed similar readings (zero) of DBP. The service engineer of the manufacturer was contacted, and the monitor was sent for service and repair.

Transient and sudden hypotension with use of fibrin glue

undergoing spine surgery in prone position. It is likely that the hypersensitivity to fibrin glue resulted in sudden haemodynamic instability. Fibrin sealants (fibrin glue/fibrin adhesive) are the plasma‐derived products, which mimic the final stage of clotting pathway resulting in the conversion of fibrinogen to fibrin. These products have haemostatic properties and act independent of patients’ clotting mechanism in the body. These products are either homologous or autologous in origin.[1] They are used to achieve haemostasis to seal tissue and to support wound healing.[2] However, the use of these products is not free from complications. Severe and fatal incidents of anaphylactic reactions and thromboembolism have been reported in literature.[3-5] The incidence of hypersensitivity reactions is extremely rare, ranging from 0.5 per 100,000 cases for all reactions to 0.3 per 100,000 cases for serious reactions.[6] The serologic screening includes qualitative and quantitative estimation of aprotinin specific IgE and IgG antibodies.[7-9] Fibrin sealants contain human protein concentrate (fibrinogen, plasminogen and factor XIII), thrombin, aprotinin and calcium chloride. It is contraindicated in individuals with a known hypersensitivity to aprotinin. In few cases, these reactions have also progressed to severe anaphylaxis. [4-6] Such reactions are seen when fibrin sealants are applied repeatedly over time or in the same sitting. Koberand colleagues reported anaphylactic reaction due to systemic administration of aprotinin where it was used for coronary artery bypass graft surgery.[10] In another case, mortality was reported because of the application offibrin glue on adural tear.[11] Here, it is important to state that even if the first contactis well tolerated, it does not exclude the occurrence of an immediate or a delayed allergic reaction.[7,8] The signs and symptoms include bradycardia, tachycardia, hypotension, flushing, bronchospasm, wheezing, dyspnoea, nausea, urticaria, angioedema, pruritus, erythema and paraesthesia. Mild reactions can be managed with antihistaminic, steroids and adrenaline. The serologic screening includes qualitative and quantitative estimation of aprotinin‐specific IgE and IgG antibodies, skin prick tests for bovine aprotinin and drug-induced lymphocyte stimulation test.[7-9] However, in the postoperative period, we did not investigate our patient for antibodies specific for aprotinin, as the patient refused to give consent for further investigations. Incidence of embolism hasalso been reported with fibrin glue, hence it should not be injected directly into the circulatory system.[4] To avoid adverse life-threatening anaphylactic reactions, Transient and sudden hypotension with use of fibrin glue!

Temperature and cisatracurium degradation: So what is new?

Sir, We read the article ‘Cisatracurium degradation: Intravenous fluid warmer the culprit?’ by Khan et al.[1] The authors administered cisatracurium through 150 cm long hotline tubing and observed that the drug failed to produce clinical effect. The authors quoted that ‘there is no report in the literature suggesting that there is a shortening of its activity or quality of action by enhanced metabolism when administered as an infusion via a channel at higher than body temperature’. However, there is enough literature to suggest that rise in temperature (body temperature or room temperature) will reduce the potency of cisatracurium as its metabolism is temperature- and pH-dependant. Tewari and Sikora[2] reported increased metabolism of cisatracurium in a patient with fever. In individuals undergoing coronary artery bypass surgery with induced hypothermia, Cammu et al.[3] found that the half-life of cisatracurium during hypothermia gets prolonged. De Winter et al.[4] studied the impact of temperature exposure on stability of drugs and found that cisatracurium is the first drug to lose its potency. The manufacturers also recommend that the drug should be stored at 2-8°C to preserve potency. The rate of loss of potency increases to approximately 5% per month at 25°C. Upon removal from refrigeration to room temperature (25°C), cisatracurium should be used within 21 days. It is a common practice to avoid the administration of drugs such as cisatracurium through hotline tubing considering its temperature-dependant metabolism. This article just upholds the well-known pharmacokinetic properties of cisatracurium, which were established more than a decade ago.

Opioids induced serotonin toxicity? Think again.

Sir, In a recently published article, ‘Cardiac arrest from tramadol and fentanyl combination’ by Nair and Chandy,[1] the authors concluded this case to be the first ever report of serotonin toxicity due to the co-administration of fentanyl and tramadol. We argue against this diagnosis as the patient did not fall into the diagnostic criteria of serotonin syndrome. The diagnosis of serotonin toxicity remains clinical one, and no laboratory test confirms the same. It is a syndrome characterised by a triad of neuroexcitatory features (neuromuscular hyperactivity, tremor, clonus, hyper-reflexia, pyramidal rigidity), autonomic hyperactivity (diaphoresis, fever, tachycardia, tachypnoea), and altered mental status (agitation, excitement, confusion).[2] According to another commonly used ‘Hunters Serotonin Toxicity Criteria’, at least one out of the following five clinical feature is required for the diagnosis of serotonin syndrome: Spontaneous clonus; inducible clonus with agitation or diaphoresis; ocular clonus with agitation or diaphoresis; tremors and hyper-reflexia; hypertonia, temperature above 38°C, and ocular or inducible clonus.[3] The patient in discussion had only agitation without any clonus, hyper-reflexia, or hyperthermia. Occurrence of ventricular tachycardia and subsequent fibrillation remain unexplained using any of the diagnostic criterias of serotonin toxicity. The same review article[3] as quoted by the authors clearly mentions that both fentanyl and tramadol are weak serotonin reuptake inhibitors (SRIs) and rarely precipitate dose-dependent serotonin toxicity in conjunction with serotonergic medications and that too only if large doses of fentanyl or tramadol are used or in susceptible individuals.[3] The patient in discussion was not on any serotonergic medications and authors had injected only 0.83 μg/kg of fentanyl and over 1 mg/kg of tramadol. They deferred injecting additional doses of fentanyl with the fear of developing chest wall rigidity, which did not appear by that time. Wooden chest syndrome usually occurs at much higher doses of fentanyl (12–15 μg/kg in an adult), or when the drug is injected at a rapid rate.[4] Lack of classical clinical presentation, the absence of administration of large doses of opioids and drug interaction with SRIs, makes the diagnosis of serotonin syndrome unlikely.