Introduction: Hypotension after Subarachnoid Block (SAB) can affect mother and foetus and can be prevented by prophylactic use of vasopressors. Phenylephrine (PE) has been a popular and effective drug as prophylaxis against hypotension. Norepinephrine (NE) is recently tried for this purpose. Aim: To compare PE infusion with NE infusion prophylactically against SAB induced hypotension during Lower Segment Cesarean Section (LSCS). Materials and Methods: This randomised clinical study was conducted in the Department of Anaesthesiology at a Tertiary Care Hospital, Ballari, Karnataka, India. The duration of the study was 12 months, from December 2018 to November 2019. A total of 156 primigravida and multigravida with singleton term pregnancy, posted for caesarean section under SAB received prophylactic infusions of either NE 5 μg/minute (group NE) or PE 50 μg/minute (group PE) immediately after SAB till end of the surgery. The primary outcome of the study was to assess the incidence of hypotension. The secondary outcomes included incidence of nausea, vomiting, hypertension, tachycardia, bradycardia and the neonatal outcomes. Related categorical and numerical variables were subjected to suitable statistical tests and analysed using Statistical Package for Social Sciences (SPSS) version 20.0. Results: The mean age of the study participants of group NE was 24.47±2.52 years and group PE was 23.91±2.63 years, respectively. The age, parity and surgical duration was comparable between the groups. The incidence of hypotension was 17.9% in group NE and 26.8% in group PE (p-value=0.182). No significant differences in total doses of vasopressors used were noted. The incidence of bradycardia in group NE was 3.8% and 21.8% in the group PE (p=0.053). No adverse events or neonatal outcomes were observed. Conclusion: The incidence of hypotension and the total dose of vasopressors administered were similar in the two groups receiving prophylactic infusion doses (NE or PE). Incidence of bradycardia was greater in the parturients receiving PE infusion.
Sir, We report the anaesthetic management of an 11-year-old male patient with multiple pituitary hormone deficiency (MPHD) posted for laparoscopic appendicectomy for acute appendicitis. History revealed that he was born with congenital left microphthalmos. Birth history and maternal obstetric history were normal. At 6 years of age, due to complaints of mouth breathing, child was subjected to magnetic resonance imaging (MRI) and was found to have frontoethmoidal encephalocoele; pituitary gland and optic chiasm were unidentifiable. Trans-nasal resection and repair of anterior cranial fossa floor was carried out with relief of symptoms. After 2 years, during work-up for complaints of delayed growth, investigations revealed MPHD (reduction in values for age of serum cortisol, insulin-like growth factor (IGF-1), adrenocorticotrophic hormone (ACTH) and thyroid hormones); pituitary was seen in the normal position in MRI. Bone age to chronological age was less by 2 years on X-ray and bone mineral density was low; child was started on growth hormone (GH) (subcutaneous), glucocorticoid, thyroid and vitamin D supplementation. Steroid supplementation was withdrawn after 2 years due to normalization of serum cortisol. Preoperatively, the child's height and weight were below normal for age (reference CDC Growth Chart) and cortisol, free T3, free T4, thyroid-stimulating hormone (TSH), IGF-1, blood glucose and electrolytes were within normal limits. The patient was kept nil orally and was on IV Ringer lactate. Informed and written consent was obtained from parents. Hydrocortisone 50 mg was given intravenously pre-induction, repeated after 8 hours. General anaesthesia was induced with fentanyl-thiopentone followed by vecuronium-facilitated intubation using a cuffed endotracheal tube (6.5 mm). Maintenance was done with oxygen–nitrous oxide and isoflurane 0.4%. Port entry sites were infiltrated with bupivacaine 0.25%. Haemodynamics were maintained within acceptable limits during pneumoperitoneum (limited to 14 mmHg) with isoflurane up to 0.8% and ventilatory rate adjusted to target end-tidal CO2 (ETCO2) of 35 mmHg. Reversal of muscle blockade was achieved using neostigmine-glycopyrolate. Extubation and recovery were uneventful. Monitoring included non-invasive blood pressure, pulse-oximetry, electrocardiogram, ETCO2 and urine output. Diclofenac (suppository) was used for post-operative analgesia. Urine output was normal and the patient resumed oral intake and routine hormonal supplements after 12 hours. Repeat evaluations of thyroid functions, blood sugar, serum cortisol and electrolytes on second postoperative day were normal (IGF-1 was not assayed). MPHD can be congenital (genetically mediated) or acquired (due to injury to hypothalamus, pituitary stalk, or anterior pituitary by space occupying lesions, infections and trauma).[1] In acquired variety, the patient is initially healthy and over years, features of pituitary insufficiency start. Atrophy of the adrenal cortex, thyroid and gonads is observed with delayed growth, hypothyroidism and tendency for hypoglycaemia. Height may be affected depending on age of onset and duration. Diagnosis of GH deficiency is indicated by low serum levels of IGF-I and GH-dependent IGF-BP3 (35.2 ng/ml initially, N182-780 at 6 years); definite diagnosis is by absent/low levels of GH in response to some stimulants.[1] Low levels of TSH, T3, T4, ACTH, cortisol, gonadal steroids, etc., are observed. Longer the duration of GH deficiency, more is the delay in skeletal maturation; bone age tends to be approximately 75% of chronologic age with deficient bone mineralization.[1] Replacement is by recombitant GH (somatropin) and correction of other hormonal deficiencies (thyroid hormone, steroids). Somatotropin is endogenous GH and Somatropin is recombinant GH. Dose adjustments are done based on growth and serum levels, which were done in the present case over 4 years. Normally, GH and cortisol (ACTH-stimulated release) are secreted in more amounts in response to surgical stimulus; TSH is not affected significantly.[2] GH stimulates release of smaller hormones, the IGF especially, the IGF-1 (from peripheral tissues) for its action. Bone mineralization and age-based bone growth can be checked and related to levels of GH/IGF-1.[3] GH deficiency affects body composition, physical performance and substrate metabolism and its replacement attenuates these effects; short-term and long-term effects of replacement may be significant.[4] It is important to remember the physiological effects of deficiency of the hormones in the peri-operative period. In the absence of adequate correction of the hormonal deficits, effects on glycaemic status, metabolism, water and electrolyte balance, immune status, etc., may be primarily affected with subsequent involvement of multiple organs. These can have a bearing on anaesthetic management of patients coming for incidental surgeries. Adequate replacement with monitoring of laboratory values in the preoperative period is imperative. Steroids in MPHD are stopped in the absence of symptoms of deficiency. Supplementation is advised during illness or preoperatively and hence hydrocortisone was administered before induction in the present case.[5] No definite technique of anaesthesia is discussed in the literature in patients with pan-hypopituitarism posted for incidental surgeries under laparoscopy. In congenital type with decreased bone growth, neuraxial blocks could be difficult or contraindicated.[6] The optimization of the hormonal levels removes risks associated with individual hormonal deficiencies and their effects on homeostasis both intra and postoperatively. Choice of anaesthetic agents and relaxants is based on the actual status of patient at the time of anaesthetic intervention. Etomidate is not the ideal choice if adrenal hyposecretion is a factor. It is advisable to consider the patient as not just being GH deficient but also hypoadrenal and hypothyroidal and take measures accordingly. Control of oxygenation and ventilation with careful monitoring of fluid administration during laparoscopy can avoid potential catastrophes associated with either low or exaggerated levels of the various pituitary hormones. Monitored optimization of hormones and careful modification of physiology in the perioperative period are thus associated with successful outcome in patients with MPHD presenting for incidental surgeries.
Magnesium sulphate, NMDA receptor antagonist, is known to reduce perioperative requirement of anesthetics and analgesics. A study was designed to assess the effect of intravenous (IV) MgSO4 on onset and recovery from spinal anesthesia and postoperative analgesic requirement in inguinal hernia surgeries.
Sir, Malignant hyperthermia (MH) is an inherited hypermetabolic disorder of skeletal muscle, triggered by potent anaesthetic agents. The incidence is between 1:10,000 and 1:150,000 adult patients receiving a general anaesthetic.[1] Early detection and use of dantrolene has reduced the mortality from 70% to <5%.[2] We report a case of perioperative suspected MH in a patient undergoing thyroidectomy. A 40-year-male with no significant clinical history including history of chronic medication was posted for subtotal thyroidectomy. His pulse rate was 84 beats/min and blood pressure measured 120/86 mm Hg. His airway and systemic examinations were essentially normal. Investigations including thyroid profile were within normal limits. After informed written consent, Tab. Diazepam 10 mg the night before and early morning of the day of surgery was administered. In the operation theatre after intravenous (IV) access, he was premedicated with Inj. Glycopyrrolate 0.2 mg and Inj. Fentanyl 100 μg. Monitoring included electrocardiogram, non-invasive blood pressure, oxygen saturation, temperature and following intubation, end tidal carbon dioxide (EtCO2). General anaesthesia was administered using Inj. Thiopentone sodium 300 mg and endotracheal intubation facilitated by Inj. Succinylcholine 100 mg. Intermittent positive pressure ventilation was instituted using closed circuit with sodalime and anaesthesia was maintained with O2-N2O, 0.4% to 1% halothane and appropriate doses of IV Atracurium. Perioperatively patient was haemodynamically stable, but after 45 min, towards the end of surgery there was sudden rise in heart rate (140/min) along with a rise in blood pressure (180/120 mm Hg), EtCO2 (90 mm Hg) and body temperature (108°F, 42.2°C, measured from oesophageal probe). To rule out lighter planes of anaesthesia, halothane 2% and top up of IV atracurium were administered, with hyperventilation but there was no respite from the above changes. Blood samples were drawn and sent for thyroid profile, serum electrolytes and serum creatinine phosphokinase (S.CPK). Anaesthetic circuit was changed to Bain's circuit and patient hyperventilated. Arterial blood gases revealed severe metabolic acidosis (pH – 7.08) and marked hypercarbia (PCO2 – 90 mm Hg). Laboratory investigations revealed marginally elevated thyroid values, gross elevation of S.CPK (3665 IU/L) and K+ (6.2 mmol/L). Patient developed gradual hypotension with range of dysrhythmias and conduction defects, including sinus tachycardia, supraventricular tachycardia, ventricular tachycardia and ventricular fibrillation. Pharmacological cardiac support, sodium bicarbonate, use of surface cooling with ice packs and cold IV fluids etc., as also electrical defibrillation was in vain and patient succumbed after 45 min of onset of the initial derangement. MH is a pharmacogenetic disorder of skeletal muscle that is associated with hypermetabolism secondary to uncontrolled increase of calcium in muscle sarcoplasm. It manifests in susceptible individuals when exposed to triggering agents, commonly an inhalational agent or Succinylcholine.[34] Speed of onset of MH reflects the rate of rise in intracellular Ca++ levels.[4] Mortality of less than 5% could be achieved by early diagnosis and use of dantrolene.[2] Except for the thyroid swelling, our patient was essentially healthy before this procedure. A sudden increase in heart rate, blood pressure, body temperature and end-tidal CO2 intraoperatively aroused suspicion of onset of thyroid storm, even though the patient was euthyroid, and not on any treatment. As the patient was (a) Not responding to appropriate resuscitative measures (b) Investigations revealed severe acidosis, marked hypercarbia, marginally elevated thyroid values and gross elevation in S.CPK and (c) We had used triggering agents like succinylcholine and halothane, we thought MH was a possible diagnosis. A clinical situation such as this can also be mimicked by thyroid storm, neuroleptic malignant syndrome (NMS) and phaeochromocytoma. Though hypertension, hyperpyrexia and cardiac arrhythmias were present, thyroid storm was ruled out as there were marginal elevations in thyroid hormones but marked elevation in EtCO2 and severe acidosis. As there was no history of any chronic drug intake or the triad of sweating, episodic headache and tachycardia, the possibility of either NMS or pheochromocytoma was remote.[45] The gold standard diagnostic test for MH is in vitro Halothane Caffeine Contracture test, the facilities for which were not available at our institute. We applied MH clinical grading scale and a total score of 46 was achieved (Serum K+ >6 mmol/L – 3 points, EtCO2 > 7.5 kpa during controlled ventilation – 15 points, inappropriate rapid increase in temperature – 15 points, Inappropriate sinus tachycardia – 3 points, Arterial pH < 7.25-10 points). A total score of 46 corresponds to MH rank of D5 which represents the clinical scenario as "very likely" of MH.[6] Though appropriate measures to treat the clinical condition were instituted, our patient succumbed due to non-availability of dantrolene sodium which is the drug of choice for MH. We conclude that a high index of suspicion must be maintained about onset of MH peri-operatively and prompt recognition, early intervention with dantrolene administration can be life-saving.
Pain after tonsillectomy is severe, and often it increases with swallowing. 67% of the children at home recalled severe pain experience in the hospital. Local anaesthetic peri tonsillar infiltration with general anaesthesia found to improve the operative conditions and provides excellent post-operative analgesia.
Propofol is well established as an i.v-induction drug in clinical anesthesia. However, pain on injection continues to be a problem, especially in paediatric patients. Various studies have been undertaken to reduce injection pain with different formulations of propofol. Propofol (MCT/LCT) is associated with less injection pain, hence this study is done to compare pain on injection on giving 0.5% dilution of propofol (MCT/LCT) versus 0.5% dilution of propofol (LCT) during induction of anaesthesia in children aged 6-12 years.
Succinylcholine is still a drug of choice for general anaesthesia practice, rapid sequence intubation and in patients having predicted difficult airway. However, it is associated with undesirable effect like fasciculation with incidence being 94%. Magnesium competes with calcium at the neuromuscular junction and inhibits release of acetylcholine and has been shown to reduce incidence of fasciculations.
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