Trouble Shooting the Arterial Blood Pressure Tracing: OVER DAMPENING & UNDER DAMPENING ▪️▪️▪️▪️▪️

Over dampened tracing 

➖➖➖➖➖➖➖➖➖

⏺May result in an under-reading of pressures 

⏺This may cause an underestimation of the systolic pressure and overestimation of diastolic pressure. 

▶️Check the transducer position as it may be too high above RA. 

▶️Kinking of the catheter at the insertion site may also cause the waveform to become dampened. 

Under dampened tracing 

➖➖➖➖➖➖➖➖➖

⏺noted by a high initial spike in the waveform 

⏺because of inadequate damping of the transducer, which causes an excessive resonance in the system. 

⏺ May result in an overestimate of systolic pressure and an underestimate of diastolic pressure. 

▶️check the transducer position. It may be too low below the RA. 

Better to re-zero the transducer to atmospheric pressures, in both of the above situations

TRAMADOL AND ONDANSETRON: THEY ARE NOT A GOOD PAIR ! ; WHY FORCING THEM TO LIVE TOGETHER ?

Tramadol- highlights 

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✔️both opioid and non-opioid modes of action. . 

(1) inhibition of noradrenaline re-uptake 

(2)increased release and decreased re-uptake of serotonin in the spinal cord, and 

(3)a weak effect on mu opioid receptors

✔️The weak, opioid effect is mediated by an active metabolite, (+)-M1 (O-desmethyltramadol), formed via the genetically polymorphic P450 CYP2D6 iso-enzyme system. The biological activity of this system is variable, and individuals may be classified as extensive or poor metabolisers of tramadol. 

✔️Tramadol’s affinity for opioid receptors is about 6000 times weaker than morphine, but the (+)-M1 metabolite has an affinity about 200 times greater than tramadol. Poulsen et al. report much higher concentrations of the (+)-M1 metabolite and greater analgesic efficacy of tramadol in extensive metabolisers compared to poor metabolisers. Also noted was a reduction of nausea, vomiting and tiredness amongst poor metabolisers

Ondansetron-highlights

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✔️Ondansetron competitively antagonises serotonin, subtype 3 (5-HT3) receptors in the CTZ and enteric neurones. 

✔️ Peripheral 5-HT3 receptors are also involved in nociceptive pathways and ondansetron may alter 5-HT3 nociceptive responses at the level of dorsal horn neurones

✔️ Ondansetron can block sodium channels in a similar fashion to local anaesthetic agents, and exhibit agonist activity at mu opioid receptors, thus resulting in a peripheral anti-nociceptive effect.

Tramadol + Ondansetron 

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✔️PONV due to Tramadol is often managed with a competitive serotonin antagonist, ondansetron

✔️ There is evidence that the concurrent use of these two drugs results in a mutual reduction of effect—tramadol is a less potent analgesic and ondansetron is a less effective as an antiemetic. 

✔️ But the effect of ondansetron on tramadol consumption diminished with time. 

✔️ De Witte et al. found a significant (50%) increase in cumulative tramadol consumption during the first post-operative hour when patients were given ondansetron along with Tramadol.

✔️ Ondansetron is, in part, metabolised by the CYP2D6 iso-enzyme system—an iso-enzyme system responsible for formation of an active tramadol metabolite that has analgesic effect . Competition for this metabolic pathway may result in a reduction in formation of the (+)-M1 metabolite of tramadol and a consequent reduction in analgesic efficacy.

DO YOU KNOW❓😳 additional points➕

✔️ There is animal and human evidence that both tramadol and ondansetron have local anaesthetic type properties.

✔️ Ondansetron was approximately fifteen times more potent than lignocaine and may well be a prototype molecule for the development of a new group of local anaesthetic agents. 

✔️ These findings are further supported in a human clinical study by Memis et al.which showed that tramadol and ondansetron both significantly reduced the pain associated with the injection of the neuromuscular blocking drug, rocuronium.

(Ref: J.H. Ye, W.C. Mui, J. Ren, T.E. Hunt, W.H. Wu, V.K. Zbuzek Ondansetron exhibits the properties of a local anesthetic. Anesth. Analg., 85 (1997), pp. 1116–1121)

✔️Tropisetron and granisetron are able to reverse an acetaminophen-mediated analgesia completely.

 

〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰

References:

Anaesthesia. 2015 Feb;70(2):209-18. doi: 10.1111/anae.12948. Epub 2014 Dec 10.

The effect of ondansetron on the efficacy of postoperative tramadol: a systematic review and meta-analysis of a drug interaction.

Stevens AJ1, Woodman RJ, Owen H.

Ondansetron Inhibits the Analgesic Effects of Tramadol: A Possible 5-HT3 Spinal Receptor Involvement in Acute Pain in Humans

Arcioni, Roberto MD*,; della Rocca, Marco MD*,; Romanò, Sarah MD*,; Romano, Rocco MD†,; Pietropaoli, Paolo MD*, and; Gasparetto, Alessandro MD*

ScienceDirect Review

Aspects of tramadol and ondansetron interactions Bruce Hammonds, David A. Sidebotham, Brian J. Anderson,

📝BRAIN TUMOURS-SYMPTOMATOLOGY

📌Contralateral signs :  are associated with lesions in the posterior frontal area (motor) or anterior parietal lobe (sensory)

📌Lesions in the dominant hemisphere: Aphasia

📌Lesions in the non dominant hemisphere: Apraxia

📌Temporal lobe lesions : Focal seizures with auras and visual field defects

📌Frontal lobe lesions : Altered cognitive functioning and subtle personality changes

📌Subfrontal lesions : Anosmia

📌Sellar and Parasellar lesions: Visual field and Acuity problems , hypopituitarism, oversecretion syndromes (Cushing Syndrome, Acromegaly)

📌Tumours in relation to Ventricular system : Hydrocephalus , Raised ICP

📌Tumours of the brainstem and cerebellopontine angle : Cranial nerve palsies , long tract signs , secondary hydrocephalus

📌Lesions of Cerebellar vermis : Truncal ataxia

📌Lesions in Cerebellar hemisphere: Appendicular signs such as incoordination and nystagmus 

Reference:

Page :617-618, Bailey and Love’s , SHORT PRACTICE OF SURGERY , 24 th edition

CHASING THE ICP..SORRY CHASING THE WELLNESS OF THE BRAIN❗️

📛In the absence of disease, ICP may rise by 50 mmHg during coughing or sneezing without noticeable neur ologic impairment. 

▶️Therefore, it is the interaction of raised  ICP with other intracranial pathology which produces the pathologic consequences, as  opposed to the rise in ICP per se.  

Monitoring of intracranial pressure (ICP)

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📛"Some patients with suspected intracranial hypertension and a decreasing level of consciousness might require invasive ICP monitoring, although its added value beyond clinical or radiological monitoring has not yet been proven"

📛Monitoring methods currently available include ventriculostomy, subarachnoid bolt, epidural sensor, and fiberoptic intraparenchymal monitor; the latter is the most commonly used.

▶️DO YOU KNOW?

📛The major drawback of intraventricular catheters is the rate of infection which is much higher than that observed using intraparenchymal probes. 

📛Additionally, interpretation of ICP data after craniectomy is difficult.

Monitoring of CBF

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▶️Normal average CBF in the human is approximately 55 ml/100g (of brain)/min, though values may vary widely across grey and white matter. The ischemic threshold for CBF is approximately 18 ml/100g/min, with 10 ml/100g/ min often considered the threshold for irreversible injury. 

📛Laser Doppler flowmetry (LDF) is a parenchymal or surface Doppler probe that measures tissue local CBF in a quantitative manner. 

📛Brain tissue oxygen tension (P bt O 2 ) monitoring allows direct measurement of focal tissue oxygen tension in a specific region of the brain. A P bt O 2  level below 10-15 mmHg has generally been the threshold identified at which outcome is worsened 

📛 Transcranial Doppler ultrasonography is a useful non-invasive monitor of cerebral hemodynamics, but has been severely disadvantaged by the inability to fix the  probe in position. 

 📛 Jugular venous bulb oximetry is a global hemispheric measure with low sensitivity for detecting regional ischaemia. 

🔹The normal SjvO 2  level is approximately 60%

🔹an SjvO 2  of < 50% for greater than 10 min has generally been considered to represent an ischemic desaturation. 

🔹High SjvO 2 levels may reflect hyperemia (typically >90%) or an inability of the brain to extract oxygen due to metabolic depression from sedative agents, poor oxygen unloading (e.g. sickle cell disease), or severe brain injury. 

📛Near-infrared spectroscopy (NIRS) 

🔹measures cerebral regional oxygen saturation by measuring near-infrared light reflected off the chromophobes in the brain, the most important of which are oxyhemoglobin, deoxyhemoglobin, and cytochrome A3. 

🔹Its major limitations include the intersubject variability, the variable length of the optical path, the potential contamination from extracranial blood, and most important, the lack of a definable threshold. 🔹Because of the thin scalp and skull in the neonate and infant, NIRS holds promise in this patient population but remains an investigative tool in its present form.

📛Microdialysis catheters, typically inserted in conjunction with an ICP or tissue Po2 monitor, allows sampling of small molecules in the interstitial fluid. 

🔹An increasing lactate/pyruvate ratio is sensitive to the onset of ischemia. 

🔹High levels of glycerol suggest inadequate energy to maintain cellular integrity and the resultant membrane breakdown. 

🔹Excitatory amino acids, such as glutamate, are both a marker for neuronal injury and a factor in its exacerbation.

🔹Currently, the microdialysis catheter is primarily used in two situations: (a) extensive subarachnoid hemorrhage where subsequent vasospasm is likely and (b) traumatic brain injury (TBI) 

▶️️At present, none of the methods available is sufficiently reliable or well tested to en able us to influence the clinical management of neurologically i njured patient with absolute certainty

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Reference:

Advanced cerebral monitoring in neurocritical care Nobl Barazangi, J. Claude Hemphill III, eurology India | October-December 2008 | Vol 56 | Issue 4

Intraoperative Neurophysiological Monitoring Second Edition Aage R. Møller

Postoperative management of adult central neurosurgical patients: Systemic and neuro-monitoring David Pfister, Stephan P. Strebel , Basel, Switzerland Luzius A. SteinerBest Practice & Research Clinical Anaesthesiology Vol. 21, No. 4, pp. 449–463, 2007 

Textbook of Neuroanaesthesia and Critical Care by Basil F Matta

Handbook of Neuroanesthesia, 4th Edition, James E. Cottrell

BASICS: POTENCY, DURATION AND ONSET OF ACTION OF LOCAL ANESTHETICS⚙

🗡POTENCY: 

👉🏿is affected by several factors including:

🔹Hydrogen ion balance

🔹Fiber size, type, and myelination

🔹Vasodilator/vasoconstrictor properties (affects rate of vascular uptake)

🔹Frequency of nerve stimulation

🔹pH (acidic environment will antagonize the block)

🔹Electrolyte concentrations (hypokalemia and hypercalcemia antagonizes blockade)

↔️Duration of action 

🔹is associated with lipid solubility. 

🔹Highly lipid soluble local anesthetics have a longer duration of action due to decreased clearance by localized blood flow and increased protein binding.

⏱ONSET OF ACTION

🔹Local anesthetics are weak bases and contain a higher ratio of ionized medication compared to non- ionized. 

🔹Increasing the concentration of non-ionized local anesthetic will speed onset. 

🔹In general, local anesthetics with a pKa that approximates physiologic pH have a higher concentration of non- ionized base resulting in a faster onset. 

🔹On the other hand, a local anesthetic with a pKa that is different from physiologic pH will have more ionized medication which slows onset. 

🔹For example, the pKa for lidocaine is 7.8 and 8.1 for bupivacaine. Lidocaine is closer to physiologic pH than bupivacaine. Lidocaine has a greater concentration on non-ionized local anesthetic than bupivacaine which results in a faster onset. 

🔹 Non-ionized and ionized portions of local anesthetic solution exert distinct actions. 

🔹 Lipid soluble, non-ionized form of the local anesthetic penetrates the neural sheath and membrane. 

🔹 In the cell, the non-ionized and ionized forms equilibrate. 

🔹 The ionized form of the local anesthetic binds with the sodium channel. Once “bound” to the sodium channel, impulses are not propagated along the nerve.

🔹 Clinically, onset of action is not the same for all local anesthetics with the same pKa. This is due to the intrinsic ability of the local anesthetic to diffuse through connective tissue. 

🔹 Local anesthetics with a pKa closest to the physiological pH generally have a higher concentration of non-ionized molecules and a more rapid onset. 

🔹 Two notable exceptions are chloroprocaine and benzocaine. Chloroprocaine has a high pKa and rapid onset. Benzocaine does not exist in an ionized form and exerts its effects by alternate mechanisms.

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#LocalAnesthetics, #RegionalAnesthesia , #Pharmacology , #anaesthesia

References

Heavner, J.E. (2008). Pharmacology of local anesthetics. In D.E. Longnecker et al (eds) Anesthesiology. 

Joyce, J.A. (2002). A pathway toward safer anesthesia: stereochemical advances. AANA Journal, 70, 63-67.

Katzung, B.G. (1992). Section 1: basic principles. In B.G. Katzung Basic & clinical pharmacology, 5th edition. Norwalk, Connecticut: Appleton and Lange.

Morgan, G.E., Mikhail, M.S., Murray, M.J. (2006). Local Anesthetics. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. 

Stoelting, R.K. & Hillier, S.C. (2006). Pharmacology and pharmacodynamics of injected and inhaled drugs. In R.K. Stoelting & S.C. Hillier (eds) Pharmacology & Physiology in Anesthetic Practice, 4th edition. 

Strichartz, G.R. & Berde, C.B. (2005). Local Anesthetics. In R.D. Miller Miller’s Anesthesia, 6th edition

AN ADULT STORY: HOW ADULTS LEARN❓

👉🏿Malcolm Knowles introduced the term “andragogy” to North America, defining it as “the art and science of helping adults learn.” Andragogy is based on five assumptions—about how adults learn and their attitude towards and motivation for learning.

👉🏿Andragogy—five assumptions about adult learning

🔹Adults are independent and self directing

🔹They have accumulated a great deal of experience, which is a rich resource for learning

🔹They value learning that integrates with the demands of their everyday life

🔹They are more interested in immediate, problem centred approaches than in subject centred ones

🔹They are more motivated to learn by internal drives than by external ones

👉🏿Most theorists agree that andragogy is not really a theory of adult learning, but they regard Knowles’ principles as guidelines on how to teach learners who tend to be at least somewhat independent and self directed.  

👉🏿His principles can be summarised as follows:

🔹Establish an effective learning climate, where learners feel safe and comfortable expressing themselves

🔹Involve learners in mutual planning of relevant methods and curricular content

🔹Involve learners in diagnosing their own needs—this will help to trigger internal motivation.

🔹Encourage learners to formulate their own learning objectives—this gives them more control of their learning

🔹Encourage learners to identify resources and devise strategies for using the resources to achieve their objectives

🔹Support learners in carrying out their learning plans

🔹Involve learners in evaluating their own learning—this can develop their skills of critical reflection.

#teaching , #learning ,#psychology ,#MedicalTeaching ,#andragogy

S͙U͙P͙E͙R͙I͙O͙R͙I͙T͙Y͙ A͙N͙D͙ E͙Q͙U͙I͙V͙A͙L͙E͙N͙C͙E͙ T͙R͙I͙A͙L͙S͙ ⬆️↔️

⬆️S͙U͙P͙E͙R͙I͙O͙R͙I͙T͙Y͙ T͙R͙I͙A͙L͙S͙

✔️Seek to establish that one treatment is better than another 

✔️The sample size is set so that there is high statistical power to detect a clinically meaningful difference between the two treatments 

↔️E͙Q͙U͙I͙V͙A͙L͙E͙N͙C͙E͙ T͙R͙I͙A͙L͙S͙

✔️Seek to test if a new treatment is similar  in effectiveness to an existing one

✔️Appropriate if the new treatment has certain benefits such as fewer side effects, being easier to use, or being cheaper 

✔️Designed to be able to demonstrate that, within given acceptable limits, the two treatments are equally effective 

✔️Equivalence is a pre-set maximum difference between treatments such that, if the observed difference is less than this, the two treatments are regarded as equivalent . The tighter the limits of equivalence are set, the larger the sample size that will be required 

✔️A serious condition requires tighter limits for equivalence than a less serious condition. 

✔️The calculated sample size tends to be bigger for equivalence trials than superiority trials 

🔴T͙H͙I͙N͙G͙S͙ T͙O͙ R͙E͙M͙E͙M͙B͙E͙R͙

👉🏿In general the design and implementation of equivalence trials is less straight forward than superiority trials 

👉🏿If patients are lost to follow-up or fail to comply with the trial protocol, then any differences between the treatments is likely to be reduced and so equivalence may be incorrectly inferred.

👉🏿So equivalence trials need very strict management and good patient follow-up to minimize these problems 

👉🏿It is often helpful to include a secondary analysis where subjects are analysed according to the treatment they actually received, ‘per protocol’ analysis 

#MedicalResearch ,#ClinicalResearch , #MedicalStatistics , #BioStatistics , #AnaesthesiaResearch , #Statistics ,#research

Reference: Oxford Handbook of Medical Statistics, Janet L. Peacock , Philip J. Peacock

ANESTHESIA INFO FROM THE LAY MEDICAL MAN- Facebook Page

XENON-THE STRANGER🌪

🍭colorless, odourless, tasteless gas

🍭four times denser than air. 

🍭density and viscosity are substantially higher than those of other inhalational anaesthetics. 

🍭occurs in extremely low concentrations (0.0875 ppm) in the atmosphere, hence its name from the Greek ‘xenos’ meaning ‘stranger’. 

🍭Xenon has been used experimentally as an anaesthetic for more than 50 years 

🍭Recently there has been a renewed interest in xenon as a safe, effective and more environmentally friendly substitute for nitrous oxide (Sanders et al. 2003). 

🍭manufactured by fractional distillation of liquefied air, currently at a cost of US $10 per litre (i.e. about 2,000 times the cost of producing N2O). This high cost is the major factor limiting its more widespread use, even when used in low-flow delivery systems. 

🍭Xenon has many of the properties of an ideal anaesthetic. 

🍭Its blood/gas partition coefficient (0.12) is lower than that of any other anaesthetic, giving rapid induction and emergence. 

🍭It is unlikely to be involved in any biochemical events in the body, and is not metabolised. 

🍭Xenon causes no significant changes in myocardial contractility, blood pressure or systemic vascular resistance, even in the presence of severe cardiac disease (Sanders et al. 2005). 

🍭The unique combination of analgesia, hypnosis, and lack of haemodynamic depression in one agent would make xenon a very attractive choice for patients with limited cardiovascular reserve 

🍭In contrast to other inhaled anaesthetic agents, xenon slows the respiratory rate and increases the tidal volume, thereby maintaining minute ventilation constant. 

🍭Airway pressure is increased during xenon anaesthesia, due to its higher density and viscosity rather than direct changes in airway resistance (Baumert et al 2002). 

🍭Because of its high cost xenon must be used in low-flow closed circuits. Crucial to this method of administration is accurate measurement of the concentration of xenon in the circuit. This measurement is generally difficult as xenon is  diamagnetic and does not absorb infrared radiation (commonly used to measure the  concentrations of other agents), and its low reactivity precludes the use of specific fuel cell or electrode-type devices. 

🍭Xenon conducts heat better than other gases, and a technique based on thermal conductivity has proved to be effective (Luginbuhl et al 2002). 

🍭Because xenon is heavier than air, the speed of sound is slower in xenon than that in air, and this difference has been also been used to measure xenon concentration. 

🍭Because xenon is a normal constituent of the atmosphere, it does not add to atmospheric pollution when emitted from the anaesthesia circuit. This is in contrast to the other inhalational anaesthetics, which have ozone-depleting potential and pollute the atmosphere when released from the anaesthesia system (Marx et al. 2001). 

🍭On a molecular basis, N2O is 230 times more potent as a greenhouse gas than carbon dioxide. N2O released as a waste anaesthetic contributes roughly 0.1% of total global warming. The lifetime of N2O in the atmosphere is long—approximately 120 years. 

🍭The anaesthetic actions of xenon are thought to result primarily from noncompetitive inhibition of  NMDA receptors (De Sousa et al. 2000), a property it shares with nitrous oxide. 

🍭In common with other NMDA receptor antagonists, xenon appears to have neuroprotective properties (Sanders et al. 2003). 

🍭Xenon is also an excellent analgesic, an action mediated by NMDA receptors (De Sousa et al. 2000). 

🍭Xenon also inhibits the plasma membrane Ca 2+   pump, altering neuronal excitability and inhibiting the nociceptive responsiveness of spinal dorsal horn neurones. 

(Reference : Jürgen Schüttler •  Helmut Schwilden Modern Anesthetics ,Handbook of Experimental Pharmacology, vol 182)

EXAMPLES OF RESEARCH QUESTIONS🔢

(From : Oxford Handbook of Medical Statistics, Janet L. Peacock, Philip J. Peacock, P:5)

❓What is the prevalence of diabetes mellitus in the population? 

🔴This is a simple descriptive study 

❓How effective is influenza vaccination in the community-based elderly? 

🔴This is a comparative study, comparing individuals who had vaccines with those who did not 

❓Does lowering blood pressure reduce the risk of coronary heart disease? 

🔴This is an evaluative study, investigating the effi cacy of lowering blood pressure 

❓Is prognosis following stroke dependent on age at the time of the event? 

🔴This is an observational study 

❓Why does smoking increase the risk of heart disease? 

🔴This is an explanatory study investigating the mechanism behind an observed relationship 

❓What evidence is there for the effectiveness of antidepressants in treating depression? 

🔴This study is a meta-analysis of existing interventional studies

STATES ASSOCIATED WITH AUTONOMIC DYSFUNCTION⚠️

💠Diabetes

💠Hypertension

💠Renal failure

💠Aging

💠Postcarotid endarterectomy 

💠Spinal cord injury

💠Shy-Drager Syndrome

💠Idiopathic orthostatic hypotension 

💠Chronic alcoholism

💠Posterior flossa tumors/surgery 

💠Guillain-Barré syndrome 

💠Malignancy

RISK FACTORS FOR POST OPERATIVE COGNITIVE DYSFUNCTION

📽---->>PROJECT THE RAYS CORRECTLY

(Basic facts about projection in X ray films)

📐Postero-anterior (PA) will not produce as much magnification of the heart and mediastinum as an antero-posterior (AP) projection. So PA films are the preferred ones.

📐A PA film is taken with the film cassette in front of the patient and the beam delivered from behind with the patient in an upright position. 

📐Portable films and those taken in ICUs are all AP projection. 

📐The supine position causes distension of the upper lobe blood vessels, which may be confused with elevated left atrial pressure 

📐A lateral X-ray is useful in localising lesions in the AP dimension, locate lesions behind the left side of the heart or in the posterior recesses of the lungs. 

📐A left lateral (with the left side of the chest against the film and the beam projected from the right) is the standard projection. 

📐The heart is magnified less with a left lateral as it is closer to the film. 

📐To visualize lesions in the left hemithorax, obtain a left lateral film and for right-sided lesions a right lateral. 

📐Expiratory films are used to assess air trapping in bronchial obstruction such as a foreign body. 

📐A pneumothorax always appears larger on an expiratory film and occasionally a small pneumothorax may only be visible on expiration. 

📐Films if accidentally taken in expiration, can result in spurious magnifcation of the heart and mediastinum.

#xray ,#radiology ,#imaging , #XrayBasics , #anaesthesia 

Reference: Radiology for Anaesthesia and Intensive Care (Richard Hopkins, Carol Peden and Sanjay Gandhi)

〽️DIAPHRAGMATIC EVENTRATION

🔹 typically affects only a segment of the hemidiaphragm

🔹 is due to incomplete muscularisation of the diaphragm with a thin membranous sheet replacing the normal diaphragmatic muscle. 

🔹 Over time this region stretches and on inspiration does not contract normally. 

🗣Sudden rupture can occur with increase in intra-abdominal pressure (e.g. coughing, straining during light anesthesia or extubation etc)

🔹True rupture (if it happens)  - Effects: 

🔹mass effect of the abdominal viscera-->direct compression of the heart, mediastinal shift 

🔹Compression of vena cava and pulmonary veins--> impairs venous return, decreased cardiac output. 

👉🏿So we should maintain adequate depth of anaesthesia 

👉🏿Avoid Nitrous oxide (expansion of intra-abdominal viscera can impair the circulation and respiration)

#DiaphragmaticEventration , #eventration , #anaesthesia , #anesthesia , #DiaphragmaticHump ,#Radiology ,#cxr ,#ChestXray

Reference: Anaesthetic Management of an Adult Patient with Diaphragmatic Eventration

Azhar Rehman*, Zafar Ali Mirza, Saad Yousuf and Asma Abdus Salam, radiopaedia.org

🔴T̠H̠E̠ B̠A̠S̠I̠C̠S̠ O̠F̠ R̠E̠S̠P̠I̠R̠A̠T̠O̠R̠Y̠ P̠H̠Y̠S̠I̠O̠L̠O̠G̠Y̠ & A̠B̠G̠🔴 A FEW POINTS

⚡️CO2  is the most important stimulus for respiration

😇Receptors for CO2  are found in the medulla of the brain (central chemoreceptors)

❤️Receptors for O2  are found mainly in carotid and aortic bodies 

👑CO2  is the more important gas as the body has more capacity to store CO2  than O2 or hydrogen ions 

1️⃣0️⃣In normal people at sea level, only 10% of the respiratory drive is due to hypoxic stimulation. 

▶️◀️Unlike the central stimulation of hypercapnia, hypoxia causes central depression of the respiratory drive. 

▶️◀️Acidosis (high H + /low blood pH) stimulates respiration; conversely alkalosis depresses it.

😳For gas exchange, the lungs provide an interface of total surface area about 55 m2 via 700 million alveoli

🎯Alveolar ventilation’ is that part of the total ventilation (i.e. all gas entering the lungs) that participates in gas exchange with pulmonary capillary blood; it is equal to total ventilation minus the ventilation of the conducting airways (i.e. dead-space ventilation).The average alveolar ventilation is about 4 L/min.

📥The alveolar–arterial oxygen gradient ( P(A-a)O2 ) is a measure of the oxygen that has reached the arterial blood supply as a ratio of the total oxygen in the alveoli. It is a useful index of pulmonary gas exchange function. 

➡️This requires that three elements are working correctly: 

⏺Circulatory anatomy is normal. Anomalies such as ASD & PDA can cause anatomical shunting,  i.e. venous blood passes through routes that are not exposed to alveolar air 

⏺Ventilation and perfusion are matched 

⏺The respiratory membrane allows sufficient free diffusion of gases between air and blood.  A diffusion defect impairs the alveolar–capillary membrane, e.g. in interstitial lung fibrosis

🔢In a healthy individual breathing room air (at FiO2 21) the PO2  in alveolar air is 104 mmHg and in arterial blood 95 mmHg . PAO2 exceeds PaO2 by 15 mmHg .Thus, at an FiO2 of 21, the P(A–a)O2 is 15 mmHg 

🎭In blood, CO2  is present as: 

✔️Dissolved in blood plasma (5.3% in arterial blood)

✔️Bound to haemoglobin as carbaminohaemoglobin within erythrocytes (4.5%) 

✔️In the form of bicarbonate attached to a base (90%) As CO2 diffuses from peri

Reference:"Understanding ABGs & Lung Function Tests"  Muhunthan Thillai, Keith Hattotuwa

RESPIRATORY STIMULANTS AND DEPRESSANTS

🏀Drugs that act as Respiratory stimulants 

⤴️Acetazolamide 

⤴️Aminophyllines 

⤴️Doxapram  

⤴️Progesterone 

⤴️Salicylates

🏀Drugs that act as Respiratory depressants 

⤵️Alcohol 

⤵️Anaesthetics 

⤵️Anticholinergics 

⤵️Antihistamines 

⤵️Barbiturates 

⤵️Benzodiazepines 

⤵️Opioids

#pharmacology , #pulmonology , #icu , #sedation , #anesthesia , #anaesthesia , #criticalcare

🤓MNEMO>

N͞͞A͞͞T͞͞U͞͞R͞͞A͞͞L͞͞L͞͞Y͞͞ O͞͞C͞͞C͞͞U͞͞R͞͞R͞͞I͞͞N͞͞G͞͞ O͞͞P͞͞I͞͞O͞͞I͞͞D͞͞S͞͞

😉P͎A͎P͎A͎ C͎a͎r͎e͎s͎ M͎O͎R͎e͎ T͎H͎a͎n͎ N͎A͎T͎U͎R͎E͎😉

PAPAVERINE CODEINE MORPHINE THEBAINE

#mnemonics ,#MedicalMnemonics , #anaesthesia

🤓MNEMO>

Do you know what CVS anomaly you have to rule out, if you get a patient with TURNERS SYNDROME, for any surgery?

😉Aorta is the vessel, which 'TURNs back'😉

Answer: Coarctation of Aorta, Aortic Valvular Disease❗️

#mnemonic ,#MedicalMnemonic

BLOODY MATCH MAKING❗️❗️❗️❗️

💋RED CELL COMPONENTS 

In red cell transfusion, there must be ABO and RhD compatibility between the donor’s red cells and the recipient’s plasma. 

❤️Group O individuals can receive blood from group O donors only 

❤️Group A individuals can receive blood from group A and O donors 

❤️Group B individuals can receive blood from group B and O donors 

❤️Group AB individuals can receive blood from AB donors, and also from group A, B and O donors

(Red cell concentrates, from which the plasma has been removed, are preferable when non-group specific blood is being transfused.)

💋PLASMA AND COMPONENTS CONTAINING PLASMA 

In plasma transfusion, group AB plasma can be given to a patient of any ABO group because it contains neither anti-A nor anti-B antibody. 

❤️Group AB plasma (no antibodies) can be given to any ABO group patients 

❤️Group A plasma (anti-B) can be given to group O and A patients 

❤️Group B plasma (anti-A) can be given to group O and B patients 

❤️Group O plasma (anti-A + anti-B) can be given to group O patients only

Reference:

THE CLINICAL USE OF BLOOD: HAND BOOK , World Health Organization & Blood Transfusion Safety , GENEVA 

#blood , #transfusion , #TransfusionMedicine ,#BloodCompatibility ,#BloodTransfusion ,#anesthesia ,#BloodDonor ,#BloodBank

BREAK THE CAMOUFLAGE ⚒ 👹DIABETES INSIPIDUS Vs 👺SIADH Vs 🤖CSWS

DIABETES INSIPIDUS (DI)

➖➖➖➖➖➖➖➖➖

🧀Absence/ ineffectiveness of ADH to concentrate urine 

🧀Leads to the passage of a large volume of inappropriately dilute urine with a consequent rise of plasma osmolality (due to disproportionate loss of water over sodium) and progressive dehydration. 

DIAGNOSIS

🧀DI is present when the urine output is excessive, the urine osmolality is inappropriately low relative to serum osmolality (which is above normal because of water loss), and the urine specific gravity is less

🧀Polyuria (more than 4 ml/kg/hr in children, more than 6 ml/kg/hr in neonates or, in an adult >250 mL/hour or 4 to 14 L/day) of dilute urine 

🧀Dehydration

🧀Hypernatremia

🧀increased serum osmolality (>295 mOsm/kg)

🧀decreased urine osmolality (<300 mOsm/kg)

🧀decreased urine specific gravity (<1.002-1.005)

TREATMENT 

Hydration

🧀The amount and content of intravenous fluids are guided by urine volume, serum electrolytes and serum osmolality. 

🧀 If fluid is replaced early, it is not necessary to administer free water (D5W). Rather, a hypotonic solution such as 0.45% sodium chloride (NaCl) or lactated Ringer's may be given. 

🧀 Insulin and potassium supplementation might be required when dextrose-containing fluids are used, especially if corticosteroids are used concomitantly. Give appropriate potassium supplementation. 

Hormonal 

🧀 If the urine output is >250-300 mL/hour for 2 hours hormonal treatment is given

🧀 Desmopressin (DDAVP), a synthetic analog of the natural hormone arginine vasopressin, is available as intranasal, oral, or IV forms. 

✔️The intranasal preparation of DDAVP delivers a 10 ug dose per spray, and doses of 10-30 ug per day are usually effective. 

✔️The IV form (4 ug/mL) is given IV, intramuscularly (IM), or subcutaneously in doses of 0.5–2 ug every 8–12 hours as needed. 

✔️Oral tablets (0.1–0.2 mg) in doses of 0.1–1.2 mg/day can also be given to obtain adequate diuresis.

✔️Vasopressin can be given subcutaneously in doses of 4–10 units every 6 hours as needed for urine output exceeding 250 mL.

✔️Alternatively, a continuous infusion can be used, as the half-life of vasopressin given IV is only 20 minutes. A dose of 0.008 – 0.04 units/kg/hour is usually effective

🧀 Once intravascular volume has been restored, persistent hypernatremia may be treated with thiazide diuretics, such as hydrochlorothiazide, 50 to 100 mg/day i.v.

Syndrome of inappropriate antidiuretic hormone secretion (SIADH). 

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🧀Various cerebral pathologic processes (mostly head trauma) can cause excessive release of ADH, which leads to the continued renal excretion of sodium (>20 mEq/L), despite hyponatremia and associated hypo osmolality. 

🧀 The key findings are urinary sodium loss without corresponding loss of water, leading to a decrease in plasma osmolality in the presence of hypertonic urine. 

Urine osmolality is therefore high relative to serum osmolality. 

🧀 Blood urea nitrogen (BUN) and serum creatinine are normal and serum uric acid is generally low.

TREATMENT 

🧀 The mainstay is fluid restriction to 1,000 mL/24 hours of iso-osmolar solution. 

🧀 If hyponatremia is severe (<110 to 115 mEq/L), the administration of hypertonic (3% to 5%) saline and furosemide might be appropriate. Because rapid correction of hyponatremia has been associated with the occurrence of central pontine myelinolysis, restoring serum sodium at a rate of approximately 2 mEq/L/hour is advisable.

Cerebral Salt Wasting Syndrome (CSWS)

➖➖➖➖➖➖➖➖➖➖➖➖➖➖

🧀 It is renal loss of sodium due to intracranial disease, leading to hyponatremia and hypovolemia. 

🧀 Raised levels of circulating ANP and BNP mediate, increased natriuresis and hyponatremia in acute brain injury

🧀 CSWS is predominantly associated with SAH but has also been described in conjunction with TBI, glioma, and tuberculous or carcinomatous meningitis.

🧀 The key distinction to be made is that patients with CSWS are clinically hypovolemic compared with the euvolemic or slightly hypervolemic status of patients with SIADH. Patients with CSWS may have abnormally elevated BUN greater than creatinine, increased hematocrit, and increased serum uric acid.

DO U KNOW❓

🧀 Hypothyroidism is another important consideration in patients with hyponatremia following pituitary surgery. It may even occur in patients who are partially treated. 

🧀 decreased cardiac output (with stimulation of baroreceptors leading to increased ADH release), decreased clearance of ADH, or resetting of the osmostat may all contribute (ref : Postoperative Care Following Pituitary Surgery, Journal of Intensive Care Medicine 20(3); 2005, P:134)

ADDITIONAL EXPLANATION: DI

🧀 In neurologic practice, it is particularly associated with pituitary surgery,Traumatic Brain Injury and anterior communicating artery aneurysmal SAH.Patients who become brain dead often develop severe DI and this is relevant in the management of potential organ donors.

🧀 Diuresis of solute may also be caused by osmotic diuresis secondary to the use of mannitol or hypertonic saline, for control of intracranial pressure, or hyperglycemia.

🧀 DONT DO THIS❗️Excess fluids are sometimes administered intravenously during the perioperative period, which are then excreted appropriately postoperatively. If this large postoperative diuresis is matched with continued intravenous fluid infusions, an incorrect diagnosis of DI may be made based on the resulting hypotonic polyuria. Therefore, if the serum [Na] is not elevated concomitantly with the polyuria, the rate of parenterally administered fluid should be slowed with careful monitoring of the serum [Na] and urine output until a diagnosis of DI can be confirmed by continued hypotonic polyuria in the presence of hypernatremia or hyperosmolality.

ADDITIONAL EXPLANATION: SIADH

🧀 The most common causes in the neurologic group include meningitis/encephalitis, brain tumor, SAH, and TBI. 

🧀 Also reported following spinal surgery.

🧀 Drug-related hyponatremia secondary to the antiepileptic drugs carbamazepine and  oxcarbamazepine 

#anaesthesia ,#neurosurgery , #endocrinology ,#pituitary , #DiabetesInsipidus , #desmopressin , #siadh 

REFERENCE:

Endocrinol Metab Clin N Am 37 (2008) 213–234Disorders of Water and Salt Metabolism Associated with Pituitary Disease Jennifer A., Joseph G. Verbalis

Newfield, Philippa; Cottrell, James E., Handbook of Neuroanesthesia, 4th Edition

Disturbances of Sodium in Critically Ill Adult Neurologic Patients A Clinical Review Martin Tisdall, MRCS, Matthew Crocker,Jonathan Watkiss and Martin Smith, (J Neurosurg Anesthesiol 2006;18:57–63)

REFINE YOUR IMPRESSION OF 📕PaO2 Vs 📗SaO2 Vs 📘CaO2

⭕️Oxygen content ( PaO2 )  is the pressure of oxygen molecules dissolved in blood, and is measured by ABG analysis with units of kPa or mmHg 

⭕️Oxygen saturation ( SaO2 )  is a measure of the percentage of haemoglobin sites that have oxygen bound, commonly measured with a pulse oximeter 

⭕️Oxygen content ( CaO2 )   is the real measure of blood oxygen quantity as it accounts for dissolved and haemoglobin bound oxygen. (i.e. CaO2 directly reflects the TOTAL number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin.  It is given as the volume of oxygen carried in each 100 ml blood (mL O 2 /100 mL). Normal CaO2 ranges from 16 to 22 ml O2/dl.

EXPLANATION:

⭕️Oxygen saturation ( SaO2 ) is expressed as the percentage of haemoglobin-binding sites that are occupied by oxygen, thereby forming oxyhaemoglobin. 

⭕️Arterial blood is normally at 97–98% O 2  saturation (i.e. 98% of the available haemoglobin is combined with O 2 ), whereas venous blood is normally at 74% O2  saturation. 

⭕️O2 constitutes 21% of the atmosphere by volume and atmospheric PO2 is 159 mmHg at sea level . At an alveolar pressure of 104 mmHg, alveolar oxygen diffuses into pulmonary venous blood and raises its O2 content from 15 mL/100 mL to 20 mL/100 mL. Of this amount 19.75 mL is combined with haemoglobin and 0.25 mL is ‘free’ or dissolved in simple solution in the plasma. At this pressure of alveolar O2 , haemoglobin in the arterial blood normally becomes 98% saturated and and 2% of the haemoglobin remains reduced, i.e. free of oxygen.

⭕️PaO2 is determined by alveolar PO2 and the state of the alveolar-capillary interface, not by the amount of hemoglobin available to soak them up. PaO2 is not a function of hemoglobin content or of its characteristics. This explains why, for example, patients with severe anemia or carbon monoxide poisoning or methemoglobinemia can (and often do) have a normal PaO2.

⭕️The most common physiologic disturbance of lung architecture, and hence of a reduced PaO2, is ventilation-perfusion (V-Q) imbalance. Less common causes are reduced alveolar ventilation, diffusion block, and anatomic right to left shunting of blood. 

⭕️Think of PaO2 as the driving pressure for oxygen molecules entering the red blood cell and chemically binding to hemoglobin; the higher the PaO2, the higher the SaO2. 

⭕️ In contrast to the other two variables, CaO2 depends on the hemoglobin content and is directly related to it; Since the dissolved oxygen contributes minimally to CaO2 under physiologic conditions, CaO2 is determined almost entirely by hemoglobin content and SaO2, and is related linearly to either variable.

CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl).

#oxygen , #spo2 , #respiration , #O2 , #pulmonology , #OxygenCascade , #anaesthesia 

Reference:

(Chapter 5 of Dr. Martin's book All You Really Need to Know to Interpret Arterial Blood Gases, 2nd edition, published February 1999 by Lippincott Williams & Wilkins, Understanding ABGs & Lung Function Tests,Pocket Tutor, Muhunthan  Thillai ,Keith Hattotuwa )

COME ON B.P.😲😲😲😲😲😲‼️

✔️The specific intraoperative situations in which induced arterial hypertension might be beneficial in Neuroanesthesia : 

(1) interventional neuroradiology (e.g.endovascular obliteration of cerebral aneurysms, cerebral angioplasty/stenting and intraarterial thrombolysis; 

(2) transient vessel occlusion during clipping of cerebral aneurysm and carotid endarterectomy

(3) extracranial to intracranial bypass surgery

(4) Surgery in patients with cerebral vasospasm after subarachnoid haemorrhage 

(5) In patients with a change in the cerebral autoregulation relationship, (e.g. intracranial pathology with mass effect, systemic hypertensive disease and traumatic brain injury.)

✔️Increase in BP is attained by vasoconstriction (rather than by increasing the cardiac output because changes in cardiac output do not affect CBF.)

✔️So intraoperatively alpha-agonist, phenylephrine is commonly used. 

✔️Others like dopamine, dobutamine and vasopressin can be used in the ICU.

#InducedHypertension , #NeuroAnaesthesia , #neurosurgery , #sah , #stroke , #anesthesia , #anaesthesia , #neurointensivecare , #criticalcare 

Reference:

Curr Opin Anesthesiol 2012, 25:548–555

Protecting the brain during neurosurgical procedures: strategies that can work, Hossam El Beheiry

👁➖BE AWARE OF AWARENESS ➖👁

💣Premeditation  with amnestic reduces the chance of awareness. Also, if awareness occurs, psychological trauma is less likely without recall. 

💣Light induction doses and liberal use of muscle relaxants ,without giving adequate concern to the depth of anaesthesia can increase the chance of awareness.

💣Better to give re-bolus with i.v. hypnotic during multiple intubation attempts. Consider using inhalation induction technique. 

💣Beta-blockers,can reduce MAC-Awake and may also decrease the likelihood of PTSD. 

💣We can consider ear plugs or headphones to reduce awareness of noises in the OR. 

💣Nitrous oxide, Ketamine and Opioids suppress cortical arousal during painful stimulation, which may reduce the probability of awareness. But BIS and other EEG monitors do not accurately predict the depth of anesthesia with these drugs. (Because, even though they produce hypnosis, they do not modulate GABA-A receptors and are associated with unchanged or increased high frequency EEG signals.)

💣Propofol, barbiturates, etomidate, and halogenated volatile anesthetic agents all modulate GABA-A receptor activity and shift the cortical EEG to lower frequencies. So, BIS and other EEG-based monitors provide strong correlation with hypnosis for this group of general anesthetics.

💣MAC for N2O & volatile anesthetics is additive (i.e. a mixture of 0.5 MAC N2O plus 0.5 MAC volatile suppresses movement in response to pain like 1 MAC volatile. The HYPNOTIC activities of nitrous oxide and volatile anesthetics are sub-additive. (i.e. a mixture of 0.5 MAC-awake N2O + 0.5 MAC-awake volatile anesthetic is not as hypnotic as 1 MAC-awake volatile. This suggests that N2O has an action which antagonizes the hypnosis induced by volatile anesthetics, perhaps via direct cortical arousal.

💣Many studies say, BIS is not useful in case of dexmedetomidine also; while some others say it will help.

#awareness , #anesthesia , #sedation , #AwarenessAnesthesia , #bis , #AwarenessSurgery 

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Reference:

 CampagnaJA,MillerKW,FormanSA:Mechanismsofactionsof inhaled anesthetics. N Engl J Med 348:2110-2124, 2003

SleighJW,BarnardJP:Entropyisblindtonitrousoxide.Canwesee why? Br J Anaesth 92:159-161, 2004 39. 

ChortkoffBS,BennettHL,EgerEI2nd:Doesnitrousoxideantagonize isoflurane-induced suppression of learning? Anesthesiology 79: 724-732, 1993 40. 

KatohT,IkedaK,BitoH:Doesnitrousoxideantagonizesevofluraneinduced hypnosis? Br J Anaesth 79:465-468, 1997

Update on Bispectral Index monitoring Jay W. Johansen,Best Practice & Research Clinical Anaesthesiology Volume 20, Issue 1, March 2006, Pages 81–99

LAB et al.....(Started working).....LOL😆😆😆😆 labetalol SAGA

〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰

💉Comes as 5  mg/mL  ampoules 

💉Infusion:  200 mg/200  mL 

     Add  200mg  [40  mL]  labetalol  to  160  mL  D5W,      NS,  LR,  or  D5/NS 

     Final  concentration:  1  mg/mL 

💉Blocks  α,  β1,  and  β2  adrenergic  receptor  sites.    

💉Decreases  heart  rate  and  peripheral  vascular  resistance.  

💉Ratio  of  alpha-‐  to  beta-‐ blockade  depends  upon  the  route  of  administration  (1:3  oral  versus  1:7  IV)  

💉Onset  of  action:  2-‐ 5  minutes  

💉Duration:  2-‐ 4  hours

💉IV  Bolus:  20  mg  over  at  least  2  minutes  as  initial  dose, may  repeat  with  doses  of  40-‐ 80  mg  q10min; Do  not  exceed  total  dose of 300 mg 

💉 Infusion:  starting  2  mg/min  (2  mL/min)  –  8  mg/min  titrated  to  response.   Do  not  exceed  total  dose  of  300

💉As  cumulative  dose  nears  300mg  IV,  duration  of  action  extends  to  nearly  18  hours.

🙀-NEW INSIGHTS: 

Antihypertensive drugs methyldopa, labetalol, hydralazine, and clonidine improve trophoblast interaction with endothelial cellular networks in vitro

B Xu, F Charlton, A Makris, A Hennessy - Journal of hypertension, 2014 

#anesthesia , #GDM , #PIH , #anaesthesia

BASIC INFO: Guillain-Barre Syndrome in Neuro Critical Care Unit

🔵is an Acute Inflammatory Demyelinating Polyneuropathy (AIDP) 

🔵There will be diffuse weakness, areflexia and albuminocytologic dissociation. 

🔵In ~60% there can be preceding upper respiratory infection or diarrhea with 30% of these cases attributed to Campylobacter jejuni  

🔵Neurologic symptoms: numbness, paraesthesias, dysesthesias and progressive, bilateral symmetric weakness that progresses over hours to days and peaks in a few weeks. 

🔵normal or hyperreflexia in the initial phase changes to  areflexia. 

🔵CSF : elevated protein without pleocytosis (albuminocytologic dissociation is seen with only in 50% of patients during their first week of illness and up to 75% by the third week)

🔵Lumbar puncture is necessary to rule out infectious diseases and malignancies. 

🔵Medical complications : Respiratory failure and need for mechanical ventilation, aspiration pneumonia, sepsis, arrhythmias, cardiac arrest, and dysautonomia. 

🔵Screening for dysphagia and frequent bedside spirometry is necessary to prevent aspiration and further respiratory compromise. 

🔵They often require narcotics, gabapentin or carbamazepine to manage their acute pain (A small portion of patients will continue to experience radicular, arthralgia or meningitic pain up to one year later.) A dual approach of psychosocial support and SSRI therapy is recommended. 

🔵 both PLEX and IVIG are effective therapies for patients with GBS. 

🔵 Patients admitted within two weeks of symptom onset, bed bound on admission, and those that have minimal comorbidities can be considered for PLEX first. 

🔵 IVIG is may be easier to administer, especially when placement of a central line is not readily available. 

🔵 A Cochrane systematic review published in 2012 concluded that PLEX is more effective than supportive care, IVIG may be slightly safer, and combination therapy was not more effective than monotherapy 

Reference :

>Jacob S, Viegas S, Lashley D, Hilton-Jones D (2009) Myasthenia gravis and other neuromuscular junction disorders. Pract Neurol 9: 364-371. 

>Hughes RA, Swan AV, van Doorn PA (2012) Intravenous immunoglobulin for Guillain-Barré syndrome. Cochrane Database Syst Rev. Wil ey Online Library 7.

>Bedside Critical Care Guide / Ramzy H Rimawi

#GBS , #GBSICU , #PLEX, #neuroicu ,#neurology ,#anaesthesia ,#anesthesiologist

THE DICTATORS OF NIGHT👑💤; NREM Vs REM COMPARISON↔️

🎭Cerebral blood flow is reduced in NREM , whereas it is markedly increased in REM

🎭Sleep walks and night terrors occur in NREM; whereas dreams occur in REM

🎭Muscle tone, especially, Upper airway muscle tone is significantly reduced in REM. 

🎭DO YOU KNOW❓The only somatic muscles working in REM are the extraocular muscles and diaphragm❗️❗️

🎭There is a shift in the autonomic nervous system in sleep, with parasympathetic nervous system predominance in NREM and especially in REM

🎭NREM is organized into four stages. In a typical night of adult sleep, Stage 1 will comprise up to 5% of total sleep, Stage 2 up to 50%, SWS ( Slow Wave Sleep= Stage 3+4) up to 20%, and REM up to 25%

🎭SWS is predominately experienced in the first third of sleep and REM in the last half of sleep. Achieving SWS has neuroendocrine significance.

〰NEW INSIGHTS〰

😴Unlike propofol, sevoflurane anesthesia has differential effects on NREM and REM sleep homeostasis. (i.e.  Total sleep deprivation resulted in significantly increased NREM and REM sleep for 12-h postdeprivation. Sevoflurane exposure after deprivation eliminated the homeostatic increase in NREM sleep and produced a significant decrease in the NREM sleep δ power during the postanesthetic period, indicating a complete recovery from the effects of deprivation)

These data confirm the previous hypothesis that inhalational agents do not satisfy the homeostatic need for REM sleep, and that the relationship between sleep and anesthesia is likely to be agent and state specific.

(Pal D, Lipinski WJ, Walker AJ, Turner AM, Mashour GA

Anesthesiology [2011, 114(2):302-310)]

😴Help your patient in getting a quality sleep on preoperative day❗️

Sleep Loss and REM Sleep Loss are Hyperalgesic

Timothy Roehrs, Maren Hyde, Brandi Blaisdell, M Mark Greenwald, Thomas Roth (SLEEP, Vol. 29, No.2, 2006)

#sleep ,#nremsleep , #rem , #SleepClinic , #SleepStudy , #AnaesthesiaSleep ,#osas ,#cpap ,#brain , #SWS

HYPOPHOSPHATAEMIA IN ICUs🌀

🔹Normal range (2.5-4.5 mg/dL),

🔹Plasma phosphate concentration < 2.5 mg/dL or 0.81 mmol/L

CAUSES:

🔹Poor Nutrition

🔹Chronic Alcoholism

🔹Diarrhoea

🔹Beta 2 Agonists

🔹Insulin 

🔹Acetazolamide

🔹Hemodialysis 

🔹Hyperparathyroidism

EFFECTS

🔹Irritability 

🔹Confusion

🔹Metabolic encephalopathy 

🔹Coma

🔹Muscle weakness 

🔹Respiratory failure

🔹Failure to wean from ventilator

🔹Dysphagia

🔹Ileus

🔹cardiac arrhythmias and cardiomyopathy.

🔹ODC shift to left

TREATMENT

🔹Asymptomatic mild-to-moderate hypophosphatemia (1-2.5 mg/dL) can be treated with oral phosphate supplementation if the gastrointestinal tract is intact. 

🔹Symptomatic or severe hypophosphatemia (< 1.0 mg/dL) should be treated with intravenous phosphate.

🔹Oral supplementation : 2.5 to 3.5 g (80 to 110 mmol) per day, divided over two to three doses.

Intravenous:

🔹The required dose of initial intravenous phosphate may vary from 2.5 to 19.8 mg/kg.

Typically, 2-5 mg/kg of inorganic phosphate dissolved in 0.45% saline is given over 6-12 hours and repeated as needed.

🔹Rapid or large infusions are dangerous : Large intravenous doses of phosphate may result in hyperphosphatemia, hypomagnesemia, hypocalcemia, and hypotension.

🔹Hyperkalemia is prevented by using sodium phosphate instead of potassium phosphate in patients with potassium levels >4 mmol/L.

🔹Do not mix with Calcium or Magnesium

🔹Daily Phosphate level monitoring should be done

#hypophosphaetemia , #phosphorous , #electrolytes , #icu , #criticalcare , #IntensiveCare

ANTICOAGULANTS OF CHOICE IN VARIOUS LABORATORY TESTS☑️

🏵ESR WESTERGREN'S

🏵COAGULATION STUDIES --> SODIUM CITRATE

🏵ESR WINTROBE'S

🏵PERIPHERAL SMEAR--> EDTA

🏵Hb , PCV --> DOUBLE OXALATE

🏵OSMOTIC FRAGILITY --> HEPARIN

🏵BLOOD SUGAR--> SODIUM FLURIDE + OXALATE

#anticoagulants , #LabTests , #laboratary , #esr , #anaesthesia , #anaesthesiologist

POSTOPERATIVE AGITATION / EMERGENCE DELIRIUM IN CHILDREN AFTER SEVOFLURANE ANAESTHESIA

 

✔️Incidence up to more than 40%

✔️Might be occurring together with EEG-changes 

✔️Methods usually tried to reduce the incidence:  addition of nitrous oxide, premedication with benzodiazepines, early extubation, switching to other inhaled anaesthetics

✔️Propofol maintenance after sevoflurane induction seems to be the best alternative.

✔️A recent study also indicates that a switch to desflurane for maintenance after sevoflurane inhalation induction reduces the incidence of emergence agitation by 50 % 

✔️ A paranoid delusion is said to be a common feature of this state of agitation. 

✔️ Information about this phenomenon should be explained to the parents before the procedure. 

#EmergenceDelirium , #Sevoflurane , #PostoperativeAgitation , #anaesthesia ,#Propofol

➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖

Reference:

MayerJ,BoldtJ,Röhm K Detal (2006) Desflurane  after Sevoflurane  inhaled  induction reduces severity of emergence agitation in children undergoing minor ear nose-throat surgery compared with sevoflurane induction and maintenance. Anesth Analg 102:400-404 22. 

Breschan C, Platzer M, Jost R et al (2007) Midazolam does not reduce emergence delirium after sevoflurane anesthesia in children. Pediatr Anesth 17:347-352

UezonoS,GotoT,TeruiKetal(2000)Emergence agitation after sevoflurane  versus propofol in pediatric patients. Anesth Analg 91:563-566 20. 

NakayamaS,FurukawaH,YanaiH(2007)propofol reduces incidence of emergence agitation in preschool-aged children as well as in school-aged children: a comparison with sevoflurane. J Anesth 21:19-23

Moos DD (2005) Sevo and emergence behavioural changes in pediatrics .JPeri Anesth Nurs 20:13-18

BE SENSIBLE ENOUGH TO SENSE SSEP (SOMATO SENSORY EVOKED POTENTIAL)!

SSEP reflect the ability of a specific neural pathway to conduct an electrical signal from the periphery to the cerebral cortex.

THIS IS WHAT WE DO:

A skin surface electrode is placed near a major peripheral mixed function (motor and sensory) nerve such as the median --> a square-wave electrical stimulus of 0.2 to 2ms is applied at a rate of 1 to 2Hz. --> The stimulus intensity is adjusted to produce minimal muscle contraction (usually 10 to 60mA) --> The resulting electrical potential is recorded at various points along the neural pathway from the peripheral nerve to the cerebral cortex.

COMMON SITES OF STIMULATION:

#Upper extremity : median and ulnar nerves at the wrist. 

#Lower extremity : the common peroneal nerve at the popliteal fossa and the posterior tibial nerve at the ankle 

#Less commonly the tongue, trigeminal nerve, and pudendal nerve have been studied.

RECORDING: 

After upper limb stimulation, potentials are recorded at the brachial plexus (Erb’s point, 2 cm superior to the clavicular head of the sternocleidomastoid muscle), the cervicomedullary junction (posterior midline of the neck at the second cervical vertebra), and the scalp overlying the somatosensory cortex on the contralateral side. 

After stimulation of the lower extremity, potentials are recorded at the popliteal fossa, lumbar and cervical spinal cord, and somatosensory cortex. It is important to record nerve and subcortical potentials to verify adequate stimulation and delineate anesthetic effects.

PLOTTING:

The SSEP is plotted as a waveform of voltage vs. time.

It is characterized by: 

#Amplitude (A), which is measured in microvolts from baseline to peak or peak to peak 

#Latency (L), which is the time, measured in milliseconds, from onset of stimulus to occurrence of a peak or the time from one peak to another

MORPHOLOGY:

described as positive (P, below the baseline) or negative (N, above the baseline) 

A waveform is identified by the letter describing its deflection above or below the baseline followed by a number indicating its latency (e.g., N20) 

INTRAOPERATIVE SSEP's, INDICATIVE OF SURGICAL TRESSPASS / ISCHEMIA INCLUDE,

a . increased latency 

b . decreased amplitude 

c . complete loss 

Any decrease in amplitude greater than 50% or increase in latency greater than 10% may indicate a disruption of the sensory nerve pathways. The spinal cord can tolerate ischemia for about 20 minutes before SSEPs are lost.

ANESTHETIC DRUGS AND SSEP

 All of the halogenated inhaled anesthetics probably cause roughly equivalent dose-dependent decreases in amplitude and increases in latency that are further worsened by the addition of 60% nitrous oxide. It is best to restrict the use of volatile anesthetics and nitrous oxide to levels below 1 minimum alveolar concentration (MAC) and not to combine the two. n If possible, bolus injections of drugs should be avoided, especially during critical stages of the surgery. Continuous infusions are preferable.

CONDITIONS ALTERING SSEP

#Hypothermia : increases latency, whereas amplitude is either decreased or unchanged. For each decrease of 1 degree C, latency is increased by 1ms. 

#Hyperthermia (4 degree C) : decreases amplitude to 15% of the normothermic value. 

#Hypotension: With a decrease of the mean arterial blood pressure (MAP < 40mm Hg), progressive decreases in amplitude are seen. The same change is also seen with a rapid decline in MAP to levels within the limits of cerebral autoregulation. 

#Hypoxia: ?Decreased amplitude 

#Hypocarbia: Increased latency has been described at an end-tidal CO 2 < 25mm Hg. 

#Isovolumic hemodilution: Latency is not increased until the hematocrit is < 15%, and amplitude is not decreased until the hematocrit is < 7%. This effect is likely caused by tissue hypoxia.

INTRAOPERATIVE USES

#scoliosis surgery & Harrington rod placement 

#spinal cord decompression and stabilisation after acute SCI spinal fusion 

#brachial plexus exploration following acute injury 

resection of spinal cord tumours, cysts & vascular anomalies 

correction of cervical spondylosis 

#resection of 4 th  ventricular cysts 

release of tethered spinal cord 

#resection of acoustic neuroma 

resection of intracranial lesions involving the sensory cortex 

resection of thalamic tumours 

abdominal and thoracic aneurysm repair

IF SSEP CHANGES SIGNIFICANTLY,  WHAT THE SURGEON AND ANAESTHESIOLOGIST CAN DO  TO DECREASE THE INSULT?

The anesthesiologist can: 

>Increase mean arterial blood pressure, especially if induced hypotension is used. 

>Correct anemia, if present. 

>Correct hypovolemia, if present. 

>Improve oxygen tension. 

>Correct hypothermia, if present. 

The surgeon can:

>Reduce excessive retractor pressure. 

>Reduce surgical dissection in the affected area. 

>Decrease Harrington rod distraction, if indicated. 

>Check positioning of associated instrumentation (e.g., screws, hooks). 

If changes in the SSEPs persist despite corrective measures, a wake-up test may be performed to confirm or refute the SSEP findings. The patient’s anesthetic level is lightened, and a clinical assessment of neurologic function is performed. The monitoring of motor-evoked potentials along with SSEPs provides a more complete assessment of neural pathway integrity. As the sensory pathways are supplied predominantly from the posterior spinal artery & the motor tracts from the anterior,  a significant motor deficit can develop without significant change in SSEP's.

ACUTE PAIN AFTER CRANIOTOMY - PEARLS💎

🗡Severe pain ( > 4 on a 0–10 scale) is commonly experienced during the first 48h with an incidence of nearly 70% on the first postoperative day and 48% on the second postoperative day 

🗡 Women, younger patients and patients who required opioid analgesics preoperatively report significantly greater levels of postoperative pain

🗡 Infratentorial procedures are associated with more severe pain than supratentorial procedures        

🗡Reduced pain has been reported with a translabyrinthine as opposed to a suboccipital approach for acoustic neuroma resection 

🗡The amount of muscle damage from resection of the temporalis and posterior cervical muscles may also influence the degree of postoperative pain 

🗡Preoperative Gabapentin, parecoxib and lornoxicam may reduce opiate-induced hyperalgesia 

🗡the addition of ondansetron to PCA has not been shown to reduce nausea and vomiting after craniotomy 

🗡evidence suggests that NSAIDs should be stopped prior to neurosurgery and avoided in patients with cardiovascular disease. 

🗡  Gabapentin given 7 days prior to surgery results in significantly lower postoperative pain scores and morphine consumption during the first 48 postoperative hours compared to phenytoin

🗡  Preoperative use of nerve blocks or local anesthetic infiltration reduces intraoperative analgesic requirements and may help to reduce pain in the early postoperative period

#craniotomy , #painmanagement, #painaftercraniotomy , #analgesia , #anesthesia ,#neurosurgery 

(Ref: Acute and chronic pain following craniotomy Alana M. Flexman, Julie L. Ng and Adrian W. Gelb, Current Opinion in Anaesthesiology 2010, 23:551–557)

❗️SEEING SIADH👁

✍Clinical euvolemia, hypotonic plasma, and less than maximally dilute urine are the clues 

✍establish normovolemia by physical examination. 

(Patients with SIADH are usually said to have normal volume status. However, they actually have excessive TBW. Unlike excessive saline, which is limited to ECF, excessive water distributes two thirds to the ICF and one third to the ECF. Thus the ECF excess is minor and not usually perceptible by clinical examination. Nonetheless, patients with SIADH have mildly increased ECV, which is sensed by the kidney. The kidney increases GFR, which causes a low uric acid, BUN, and creatinine. The increased ECV also increases ANP and, along with increased GFR, promotes natriuresis.)

✍measure P osm ,U osm ,P Na ,U Na , and U K . 

✍exclude pituitary, adrenal, and thyroid dysfunction 

✍Confirmatory criteria of SIADH include low P Na ( < 135 mEq/L), low P osm ( < 280mOsm/kg), U osm greater than 100mOsm/kg, U Na greater than 40mEq/L, and [U Na + U K ] greater than P Na . 

#SIADH , #anesthesia

D for DANTROLENE🔅

✔️Dantrolene inhibits calcium release via RyR1 antagonism and impairs calcium-dependent muscle contraction. 

✔️This rapidly halts the increases in metabolism and secondarily results in a return to normal levels of catecholamines and potassium. 

✔️Dose is 2 mg/kg; repeat every 5 minutes until vital signs normalise , to a total dosage of 10 mg/kg if needed. 

✔️dantrolene takes ~ 6 minutes to have any effect

✔️The solution is prepared by mixing 20 mg of dantrolene with 3 g of mannitol in 60 ml of sterile water. 

✔️Since dantrolene is relatively insoluble, preparation is tedious and time consuming, and its preparation should not be the responsibility of the primary anesthesiologist involved in the patient’s management. (May occupy several nurses)

✔️All patients who develop MH, require at least 24 hours of posttreatment management in a critical-care setting as there is chance of reappearance of symptoms ( known as recrudescence )

🔸In the ICU, continue @1mg/kg q6h for 24 hours 

🔸may be given enterally if GIT functioning  (price ~ 1000 x  less)

✔️the actions of dantrolene include:

🔸 release  of Ca ++  from the SR, without affecting re-uptake

🔸 ? antagonises the effects of Ca ++  at the actin/myosin - troponin/tropomyosin level 

🔸muscular weakness, which may potentiate NMJ blockade ~ 5-15 mg/kg produces significant muscular relaxation 

🔸there is no  effect on NMJ transmission 

🔸up to 15 mg/kg there is no  significant effect on the CVS 

🔸up to 30 mg/kg there is no  significant effect on respiration

#dantrolene , #MalignantHyperthermia, #mh ,#anaesthesia

THE RIGHT WAY OF ADMINISTERING BLOOD PRODUCTS 💧💧💧💧💧 [ from "THE CLINICAL USE OF BLOOD: HAND BOOK , World Health Organization & Blood Transfusion Safety , GENEVA ]

✔️Prefer a larger cannula: A doubling of the diameter of the cannula increases the flow rate of most fluids by a factor of 16. 

✔️In case of Whole blood, red cells, plasma and cryoprecipitate 


>Use a new, sterile blood administration set containing an integral 170–200 micron filter 

>Change the set at least 12-hourly during blood component infusion 


>In a very warm climate, change the set more frequently and usually after every four units of blood, if given within a 12-hour period 

✔In case of Platelet concentrates 

>Use a fresh blood administration set or platelet transfusion set, primed with saline. 

✔️WARMING BLOOD:

>There is no evidence that warming blood is beneficial to the patient when infusion is slow. 

>At infusion rates greater than 100 ml/minute, cold blood may be a contributing factor in cardiac arrest. However, keeping the patient warm is probably more important than warming the infused blood. 

>Warmed blood is most commonly required in: 


[1]Large volume rapid transfusions: 

    -Adults: greater than 50 ml/kg/hour 
     -Children: greater than 15 ml/kg/hour 

[2]Exchange transfusion in infants 
 

[3]Patients with clinically significant cold agglutinins. 

>Blood SHOULD ONLY BE WARMED in a blood warmer. Blood warmers should have a visible thermometer and an audible warning alarm and should be properly maintained. 

>Blood should never be warmed in a bowl of hot water as this could lead to haemolysis of the red cells which could be life-threatening. 

✔️Severe reactions most commonly present during the first 15 minutes of a transfusion. All patients and, in particular, unconscious patients should be monitored during this period and for the first 15 minutes of each subsequent unit. 

✔️The transfusion of each unit of the blood or blood component should be completed within four hours of the pack being punctured. If a unit is not completed within four hours, discontinue its use and dispose of the remainder through the clinical waste system. 



















DESMOPRESSIN

ADMINISTRATION  ROUTES: IV,  IM,  SC,  Intranasal DDAVP/Desmopressin

INDICATIONS: 

1. Treatment  of  central  diabetes  insipidus 2. Prevention  and  control  of  bleeding  (primarily  when  there  are  thought  to  be platelet  function  defects  especially  uraemia,  clopidogrel  or  cardiopulmonary bypass  -related)

 PRESENTATION AND ADMINISTRATION: 

IV: Minirin  4mcg/ml  injection Octostim  15mcg/ml  injection Doses  of  4mcg  or  less  should  be  administered  undiluted  by  direct  IV  injection.    For small  doses  (eg  0.4mcg),  4mcg  can  be  diluted  in  10  ml  of  normal  saline. For  doses  of  greater  than  4mcg  in  adults  or  children  weighing  more  than  10kg,  dilute with  50ml  of  normal  saline  and  infuse  the  first  5ml  slowly  over  5  minutes.    For  children weighing  less  than  10kg,  dilute  in  10ml  of  normal  saline  and  infuse  the  first  1-2ml  over  5 minutes.    If  no  marked  tachycardia  or  other  adverse  effects  are  observed,  give  the remainder  slowly  over  15  minutes PO: Minirin  0.1mg  tablets  (white)

 Nasal  Spray: Desmopressin  spray  (10mcg/dose),  Minirin  spray  (10mcg/dose),  Octostim  (150mcg/ dose) 

DOSAGE: 

IV: Central  diabetes  insipidus: 0.4mcg  repeated  as  required  (may  increase  the  dose  if  there  is  an  adequate  response)

 Prevention  and  control  of  bleeding: 0.3mcg/kg  (max  24mcg)  over  30  minutes  (once  only) Note:  although  IM  and  SC  routes  can  be  used,  IV  is  generally  the  preferred  route. PO: 0.1mg  -1.2mg  daily  depending  on  indication  (rarely  used  by  this  route  in  ICU)

 Nasal  Spray: Not  generally  administered  by  this  route  in  ICU

No adjustments needed in CRF

CLINICAL  PHARMACOLOGY: Desmopressin  is  a  synthetic  analogue  of  the  natural  pituitary  hormone  arginine vasopressin  (ADH),  an  antidiuretic  hormone  affecting  renal  water  conservation..

 CONTRAINDICATIONS: 

1. Hypersensitivity  to  desmopressin 2. Hyponatraemia

 WARNINGS 

When  desmopressin  acetate  injection  is  administered  to  patients  who  do  not  have  need of  antidiuretic  hormone  for  its  antidiuretic  effect,  in  particular  in  paediatric  and  geriatric patients,  fluid  intake  should  be  adjusted  downward  to  decrease  the  potential  occurrence of  water  intoxication  and  hyponatraemia.

 Particular  attention  should  be  paid  to  the  possibility  of  the  rare  occurrence  of  an  extreme decrease  in  plasma  osmolality  that  may  result  in  seizures  which  could  lead  to  coma. 

Laboratory  Tests:

 Laboratory  tests  for  monitoring  the  patient  include  urine  volume  and  osmolality.  In  some cases,  plasma  osmolality  may  be  required.

NB: may  cause  minor  increases  in  blood  pressure  requiring  changes  in  levels  of vasopressor  support. 

ADVERSE  REACTIONS 

 transient  headache,  ischaemic  stroke,  changes  in  blood  pressure  causing  either  a  slight  elevation  or  a  transient  fall  and  a compensatory  increase  in  heart  rate,  myocardial  infarction, nausea, abdominal cramps, water  intoxication  and  hyponatraemia,Local  irritation  at  site  of  injection,  thrombotic  events

LAPAROSCOPIC MYOMECTOMY; INSIGHTS FOR THE ANESTHESIOLOGIST

# Preoperative treatment with GnRH analogue to shrink the fibroid

# Surgeon may intraoperatively inject dilute Vasopressin ( 1 IU in 100 mL RL) to reduce bleeding. IV Vasopressin can cause raised BP, myocardial ischemia, arrhythmias etc

# Position: Dorsal lithotomy; steep Trendlenberg to move the bowel out of surgical field

# Surgical time :1-4 hours; EBL: 100-600 mL

# Complications: 

Puncture of major vessel/ severe bleeding 

Insufflation in the wrong place

Air Embolism

Need for conversion to laparotomy

Peroneal nerve damage from positioning

# Pain score : 4-6

#laparoscopy,#laparoscopyanaesthesia,#myomectomy, #anaesthesia, #anaesthetist

ANAESTHETIC MANAGEMENT OF SURGICAL PROCEDURES UNDER ECMO

The plastic components of the bypass circuit can sequester varying amounts of intravenous anesthetic agents resulting in unpredictable effects and side effects 

Volatile anaesthetics are not usually available on ECMO circuits due to the difficulties in scavenging 

Since anesthetic agents can alter preload and afterload, should be ready for volume replacement and administration of vasoactive agents

Should inform the perfusionist before changing the height of the surgical table, as this can alter the venous return to the ECMO circuit ( passive gravity assisted drainage)

SYRINGOMYELIA- ANESTHESIA IMPLICATIONS "SAB"

# sensitive to muscle relaxants

# autonomic hyperreflexia , avoid suxamethonium

# bulbar palsy

ATROPINE ; A VERY FAMILIAR ?STRANGER!

ATROPINE ; A VERY FAMILIAR ?STRANGER!

💧Atropine produces complete vagal block at a dose of 3 mg; 

💧should be avoided in pyrexial children, as it inhibits sweating ; 

💧delirium is another side-effect ; 

💧patients with Downs syndrome may show resistance to atropine; 

💧parenteral atropine wont cause significant pupillary dilatation and so is not contraindicated in glaucoma.

An approach in dealing with accidental Aretynoid dislocation after endotracheal intubation

Follow up the patient:

If voice is not improving: (Better to call the ENT Surgeon to do this-) Do a laryngoscopy and using any instrument, just give a mild pressure on aretynoid; usually it will fall back to correct  position.

If speech is improving,  advice VOCAL CORD ADDUCTION EXERCISES

🉐 Standing position.. Take a deep inspiration 

   and stop..and hold the breath.. this closes glottis..now strongly fall over and push against a wall...keep it for a few seconds.. Repeat this a few times.. This can force the aretynoid back to normal position by a stretching force... Usually voice is regained by this after 2 days.. 

🉐Or lift heavy weights after deep inspiration (not for CAD patients) 

🉐Plus continue Speech Therapy

Problem occurs, when Aretynoid dislocates, and nobody attempts to relocate it, and it get fixed in that position..

Intracranial Electro Corticogram(ECOG) and Anesthetic agents

Intracranial Electro Corticogram(ECOG) is an invasive EEG monitoring using subdural grids/strips or depth electrodes. Depth electrodes are an excellent modality designed to study electrical discharges from deep grey matter.

Placement of these electrodes needs general anaesthesia. Once the electrodes are inserted, the patient can have a further period of telemetry. 

With this information, the seizure focus can be defined with greater accuracy and it is also possible to undertake functional mapping of the cortical areas studied.

During resective epilepsy surgery intraoperative ECOG helps to guide the resection.

☀️Propofol is the commonly used induction agent

☀️nitrous oxide :  controversial (?decreases the spike activity significantly in some studies)

☀️remifentanil infusion enhances spike activity in the epileptogenic zone. So it can be used during ECOG monitoring

☀️Sevoflurane has greater neuro excitatory properties than isoflurane, however, the wide spread irritative response to sevoflurane is not useful in localizing the epileptogenic area. Therefore it may not be suitable for ECOG monitoring during surgery.

☀️Patients who are on long term treatment with phenytoin and carbamazepine may have increased fentanyl requirements and may be resistant to non- depolarising relaxants.

NALOXONE DOSAGE

DOSAGE: IV: For  reversal  of  post-operative  respiratory  depression  and  coma:    20-40mcg  IV  PRN 

For  opioid  overdose:    40-400mcg  IV  PRN 

Infusion:    If  an  infusion  is  required,  commence  the  infusion  with  an  hourly  infusion  rate calculated  as  2/3rd  of  the  total  bolus  dose  given  to  achieve  the  desired  opioid  reversal effect 

DOSAGE IN RENAL FAILURE AND RENAL REPLACEMENT THERAPY:   Dose  as  in  normal  renal  function    

 DOSAGE  IN  PAEDIATRICS: IV: For  post-operative  respiratory  depression  or  over-sedation,  give  0.002mg/kg/dose  (i.e. dilute  0.4mg  to  20ml  and  then  give  0.1ml/kg/dose).    Repeat  every  2  minutes  x4  if required,  then  commence  infusion  by  adding  0.3mg/kg  to  30ml  5%  dextrose  and running  at  0-1ml/hr  (0.01mg/kg/hr).   For  opiate  overdose,  give  0.01mg/kg  (max  0.4mg)  (i.e.  dilute  0.4mg  to  10ml  and  give 0.25ml/kg/dose).    Repeat  every  2  minutes  x4  if  required,  then  commence  infusion  by adding  0.3mg/kg  to  30ml  5%  dextrose  and  running  at  0-1ml/hr  (0.01mg/kg/hr