‘Thiopentone can be safely used in nead injury. ‘Thiopentone is cerebroprotective: It decreases cerebral blood flow (CBF), thus lowering intracranial pressure (ICP). It reduces cerebral oxygen consumption (decreased CMROz). It also has anticonvulsant Property Whien Is advantageous in neurosurgical patients who are at Increased risk of seizures. cer 1cP emRoz Seizure ‘Thiopentone a a a ue Ketamine " " 1 1 Halothane, 7 7 4 4 Nitrous oxide 1 1 1 1 Robin Hood or reverse steal phenomenon is seen with thiopentone. Ht constnets tne cerebral vasculature, causing a decrease In cerepral blood flow, cerebral blood volume, and Intracranial pressure. But, this cerebral vasoconstriction occurs only in normal areas. The blood vessels in the fachemic area remain dilated due to ischemia induced vasomotor paralysis and are not affected by thiopentone. This loads to redistribution of bleed flew from nermal to ischemic areas in the brain. This is called ine Robin Hood phenomenon, Intravenous Induction agent of choice in hypotension |s Ketamine = etomiaate, Ketamine helps to maintain arterial pressure, neart rate, and carciac output due to central stimulation of the ‘sympathetic nervous system and inhibition of the reuptake of norepinephrine. ‘The most epileptogenic intravenous induction agent is etomidate. Etomicate nas been associated with grand mal seizures and produces increased EEG activity In eplleptogenie foci. This feature has proven userul for intraoperative mapping of seizure foci before surgical abiation ‘Thiopentone and proporol nave anticonvulsant properties which are advantageous in neurosurgical patients who are at increased risk of seizures. Ketamine nas a mixed eect on seizure activity, with elther strong pro-convulsant or strong anticonvulsant action. Propofol is an intravenous induction agent that can be additive because of iis hypnotic property ana development of tolerance on prolonged use. ‘The abuse potential is common among health care workers with reports of selt-administration. Note: Ketamine aiso fas the potential for abuse and adaiction. Trivia: The deatn of music icon, Michael Jackson has been attributed to Propofol intoxication, administered by his personal physician. Though this powerful drug is one of the greatest boons to the field of anesthesia, administering it without adequate justincation, expertise and equipment (to manage airway) can lead to casuatties. Ketamine causes hypertension due to central stimulation of the sympathetic nervous system and inhibition of the reuptake of norepinephrine. Hence It Is useTul In patients in shock ‘Thiopentone, propofol, and etomidate produce a fall in arterial blood pressure. Etomidate has the highest incidence (40%) of postoperative nausea and vomiting (PONV) among the Intravenous anestnetes. Propofol nas antiemetic properties tnereby reducing PONV.Etomiaate nas a very nigh incidence of myoclonus ~ 30-60%. ‘This myocionus can be minimized by premedication with benzoaiazepines oF opiates. ‘Oiner potential adverse errects of etomicate: + Adrenccortical suppression + Post operative nausea ang vomiting = Seizure precipration + Pain on injection Ketamine has been associated with emergence reaction/delirium incidence of which ranges from 3% to 100%, Emergence reactions seen with ketamine include vivid dreaming, extracorporeal experiences (sense of floating out of the body), and illusions (misinterpretation of a real, extemal sensory experience) during emergence from anesthesia. These are usually asseciated with excitement, confusion, euphoria, and fear Emergence reaction can be reduced by the use of benzodiazepines. Ketamine co2s not ellett pain on injection, instead produces protcund analgesi Propofol is formulated as a lipid emulsion. whien causes pain on injection. A new aqueous proarug. fospropofol is associated with less pain on injection Etomidate, attnougn It causes pain on injection, the lpia formulation of etomidate Is associated witn a much, less frequent incidence of pain. ‘Thiopentone at a concentration greater than 2.5% can produce pain on Injection and venous thrombosis. In December 2013, the government of Inala, In response to nsing recreational use ana tne use oF ketamine as a date rape crug. has added it to Schedule X of the Drugs and Cosmetic Act requiring a ‘special license for sale and maintenance of records of all Sales for hwo years, Hallucinations and vivid dreams during recovery trom anesthesia are a manifestation of emergence: reactions rollowing ketamine. ‘The Incidence of te psychic emergence reactions ranges from 8% to 100% and are usually associates with ‘excitement, contusion, euphoria, and fear ‘The symptoms usually appear in the first hour of emergence and subside within several hours. Emergence reaction can be reduced by the use of benzodiazepines, ‘The alagnosis 1s propofol infusion syndrome. Proporol infusion syndrome is 2 rare but lethal syndrome seen when the dose of propofol infusion is greater than 4 mg/kg/hour for 48 hours or longer This syncrome Is common in children and cnitically i aautts + Acute retractory praayearaia leacing to asystole In the presence of one of more of the following ‘¢ Metabolic acidosis (base deficit >10 mmol/L) © Rnabdomyelysis, © Hyperlipidemia © Enlarged or fatty tive + Otner features - cardiomyopathy with acute cardiac failure, skeletal myopathy, hyperkalemia, hepatomegaly, and lipemia = The symptoms and signs are the results of muscle injury and the release of intracelular toxic contents. = ICs due to defect in mitoehonari I metabolism and electron transpert chain function,Dantrolene sodium is the drug of choice for malignant hyperthermia but it is to be reconstituted with ‘sterile distilled water, not saline as il can precipitate in saline or other salt solutions. It is given al a dose of 2.6 mg/ kg intravenously and can be tepeated every 5-10 minutes (upto 10 mg/kg) till the attack subsides, All anesthetic agents should be cut off and the patient is given 100% oxygen. Bicarbonate at a dose of 1 to 4 mEq/kg IV can be used to treat metabolic acidosis. If the body temperature is high, it should be brought down using cold intravenous fluics, cooling body cavities with sterile iced Mlulds, surface cooling with ice packs and cooling blankets. Destturane, being an inhalational anesthette, 1s a triggering factor tor malignant hyperthermia, Pearl #183: Malignant hyperthermia key features Pathophysiology: = Prolonged opening of functionally altered ryanodine receptors, leading to uncontrolled welease of Calcium trom the sarcoplasmic reticulum feaulting in sustained muscie contraction. = increased sympathetic activity: Tachycardia, hypertension, arrythmia. 1 Muscle damage: Masselcr spasm, generalised ngidily, hyperkalemia, rapdomyolysis, myogiobinurla o Fever, sweating + Hyperventiiation with 100% O2 + Dantrotene: 2.5 maika intravenously every 6 min until the episode Is terminated (upper limit 10. mares) + Correction of acid-base, electrolyte abnormality 2 Gosling the patient Hyperthermia is a late sign of matignant hyperthermia Clinical Manifestations of Malignant Hyperthermi: Early signs: Elevated end-tidal carbon dioxide: ‘Tachypnea anqor tachycaraia Masseter spasm, if succinyicnoline nas been used Generalized muscle rigiaity. Mixed metabolic and respiratory acidosis: Profuse sweating Mottting of skin Cardiac arrhythmias Unstable blood pressure Late signs Hyperkatemia Rapid increase of core body temperature. Doay temperature rises by 1°C every 5 minutes Elevated creatine phosphokinase levels Gross myogiobinemia and myogiobinuria Diceeminated intravascular coagulation