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Wednesday, January 18, 2017

TURP SYNDROME AND THE ANESTHESIOLOGIST

🚩#TURPsyndrome is diagnosed based on clinical signs, symptoms and biochemical findings 
🚩The manifestations are due to hypervolemia, hyponatremia and due to the direct toxicity of the irrigation fluids like 1.5% glycine
▪️FACTORS INCREASING THE ABSORPTION OF THE IRRIGATION FLUID ( AND THUS CONTRIBUTING TO THE HYPERVOLEMIA )
🚩Long duration of the surgery: the irrigation fluid is absorbed at the rate of 20-30 mL/ min and so the volume absorbed increases with the duration of the surgery 
🚩High pressure delivery of the irrigation fluid especially from a considerable height; 
The minimum height required for adequate flow should be used (usually 70 cms)
🚩Low venous pressures 
🚩Excessive bleeding (= there are more open veins)
🚩Large prostate (>50g)
▪️CLINICAL FEATURES:
🚩Headache, Restlessness, Agitation, Confusion, Convulsions, Coma; pulmonary oedema may also set in. If patient is under general anesthesia, these symptoms will get masked.
▪️MANAGEMENT FROM SURGICAL SIDE:
🚩Coagulating bleeding points and terminating surgery as soon as possible.
▪️ANESTHETIC MANAGEMENT: 
🚩Reduce / stop fluid administration. Diuretics may be required in the presence of pulmonary oedema
🚩Intubation to protect the airway and mechanical ventilation to support respiration may be required 
🚩Anti-convulsants, if needed, to treat seizures
🚩Hypertonic saline should be considered for severe hyponatremia (<120 mmol L−1) or in the presence of severe neurological symptoms.
👉🏿N.B.- Central pontine myelinolysis or osmotic demyelinating syndrome (ODS) is more likely to occur with correction of serum Na greater than 8-12 mMol/day and in the setting of chronic hyponatremia (greater than 48 h)
👉🏿Faster rates of administration can potentially lead to central pontine myelinolysis. Treatment should stop once symptoms have resolved or the serum sodium is more than 125 mmol L−1. Such therapy is best delivered in a high-dependency environment.

Thursday, January 12, 2017

BISPECTRAL INDEX



💆The EEG bispectrum is a high-order statistical computation derived from the analog EEG.

💆The BIS is a combination of three weighted parameters: (i) the burst suppression ratio (the proportion of isoelectric EEG signal in an epoch); (ii) the beta ratio (a measure of the proportion of signal power in the high vs medium frequency range); and (iii) the SynchFastSlow (relative synchrony of fast and slow waves)

💆Changes in frequency and power alone ( as done with conventional power spectral analysis) have been shown to be inconsistent when attempting to measure anesthetic depth.

💆Bispectral analysis incorporates information on power and frequency with the phase coupling information that is more indicative of anesthetic depth but not present in other clinical applications of EEG.

💆The BIS uses a combination of EEG subparameters that were selected after analysis of a large database of EEGs to demonstrate specific ranges for varying phases of anesthetic effect

💆These parameters were then combined to form the optimum configuration for monitoring of the hypnotic state.

💆The BIS is then displayed as a dimensionless number between 0 and 100 with the lower numbers corresponding to deeper levels of hypnosis.

💆There are normal, genetically determined low-voltage EEG variants among the population that can result in abnormally low BIS values in awake patients; therefore, it is important to obtain baseline values before the induction of anesthesia

💆BIS is not able to predict movement in response to surgical stimulation because the generation of reflexes is likely to be at spinal cord rather than cortical level

💆BIS does not fully reflect the synergistic effect of opioids with hypnotic agents

💆The presence of electromyographic artefacts, poor signal quality, and electrical artefacts such as those from electro-cautery and forced air warming units can cause spurious values to be displayed by the BIS monitor.

💆With the administration of ketamine, the BIS may remain high, possibly due to the excitatory actions of ketamine, and, therefore, the BIS monitor is not reliable when used to monitor hypnosis with ketamine.

💆There have been studies in which the BIS monitor has not been shown to reflect the hypnotic contribution to the anesthetic by nitrous oxide.

💆Potential benefits from the routine use of the BIS monitor include

➖decreased risk of awareness

➖improved titration of anesthetic agents and

➖decreased recovery room time

💆The BIS also gives the anesthetist additional information to consider when selecting drugs for interventions, for example, when making the decision whether to deepen anesthesia with a volatile agent, add more analgesia with an opioid, or use a vasoactive drug.

💆Also note:

➖The BIS may drop after giving a neuromuscular blocking agent if excessive EMG was present prior to giving it.

➖Ischemia attenuates the amplitude and frequency of the EEG signal, which may result in a decrease in BIS

➖Hypothermia decreases brain activity, and may decrease BIS

➖Muscle shivering, tightening, twitching etc may increase EMG and increase BIS

➖Artifacts in the higher frequency ranges [e.g. use of any mechanical device that could generate high frequency activity like patient warmer]can artificially increase the BIS value

➖Is the BIS decreasing when you think it should be increasing? Think of Paradoxical Delta pattern (characterized by a pronounced slowing of the EEG) which occurs over a short period of time (2-3 minutes).

➖If the sensor is placed over the temporal artery, pulse artifacts can cause the BIS value to be inappropriately low. Check EEG waveform for presence of pulse artifacts and move sensor if necessary.

➖Blinking or rolling his/her head by the patient, may cause artifacts that mimic slow frequency EEG patterns.

Reference: The BIS monitor: A review and technology assessment, James W. Bard, AANA Journal/December 2001/Vol. 69, No. 6

Wednesday, January 11, 2017

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

😐(Explicit = Fully and clearly expressed)

😐(Implicit =Implied or understood though not directly expressed)

😐The incidence of awareness is around 0.1–0.2%

😐Explicit Awareness is intentional or conscious recollection of prior experiences as assessed by tests or recall or recognition, which are also called direct memory test.

😐Implicit Awareness is perception without conscious recall. The patient denies recall, but may remember “something” under hypnosis.

😐Awareness (deliberate)
Surgery conducted under local or regional anaesthesia. During some neurosurgical procedures, the patient is woken up to assess whether surgery has affected, or will affect, important areas.

😐STAGES OF AWARENESS ( Griffith and Jones )

1. Conscious perception with explicit memory;
2. Conscious perception without explicit memory;
3. Dreaming;
4. Subconscious perception with implicit memory;
5. No perception and no implicit memory.

😐CAUSES

🔻may result from a failure of the apparatus to deliver adequate concentrations of anesthetic agent. Such failures include leaks, faulty or empty vaporizers, a misconnected or disconnected breathing system, inaccurate pumps, misplaced venous cannula and occluded infusion tubing

🔻may result from a failure of the clinician  to monitor the concentrations of inspired and expired volatile agents may result in inadequate anesthetic agent being delivered. TIVA is more difficult to monitor in this respect.

🔻may result from an inadequate dosing of the anesthetic agent as represented by the alveolar concentration (it is important to remember that the MAC value that is quoted is only the MAC 50 ) or the computed blood concentration in target-controlled infusion (TCI).

🔻may result from an altered physiology or  pharmacodynamics in the patient e.g. Anxiety may increase dose requirements

🔻may result from the wearing off of the induction agent during a difficult intubation sequence or with the anesthetic techniques for rigid bronchoscopy

😐CLINICAL SIGNS

🔻In the spontaneously breathing patient who is not paralyzed, awareness may be manifest by purposeful movement.

🔻Sympathetic stimulation: the main clinical signs are tachycardia, hypertension, diaphoresis and lacrimation; but their absence does not exclude awareness.  Attempts have been made to quantify these objectively by using the PRST scoring system (blood Pressure, heart Rate, Sweating, Tear formation)..

😐SEQUELAE:

Commonest is the occurrence of a post-traumatic stress syndrome, whose typical features may include nightmares, insomnia, panic attacks and agoraphobia.

😐CHECKLIST FOLLOWING A COMPLAINT OF AWARENESS DURING GENERAL ANAESTHESIA

1. Visit the patient as soon as possible, along with a witness (Preferably a consultant)
2. Take a full history and document the patient’s exact memory of events
3. Attempt to confirm the validity of the account
4. Keep your own copy of the account
5. Give a full explanation to the patient
6. Offer the patient follow-up, including psychological support, and document that this has been offered
7. Reassure the patient that they can safely have further general anaesthetics, with minimal risk of a further episode of awareness
8. If the cause is not known, try to determine it
9. Notify your medical defence organisation
10. Notify your hospital administration
11. Notify the patient’s GP


#awareness , #ptsd , #AnesthesiaComplications , #TheLayMedicalMan , From www.facebook.com/drunnikrishnanz , partial reference from frca.uk , #anaesthesia


Tuesday, January 10, 2017

Tapentadol



🚩Is a new centrally acting analgesic that relies on a dual mechanism of action. These are mu opioid receptor agonism and norepinephrine (noradrenaline) reuptake inhibition

🚩It  is  therefore  not  a  classical  opioid,  but represents  a  unique  class  of  analgesic  drug  (MOR-NRI).

🚩It  is  now  registered  for  use  in  the  treatment  of  moderate to severe chronic pain that proves unresponsive to conventional non-narcotic medications in many countries.

🚩Tapentadol  has a  much  lower  affinity  (20  times  less) to  the mu  receptor than morphine,  but its analgesic effect is only around three times less than morphine.

🚩This discrepancy is explained by its inhibitory effect on norepinephrine reuptake, strengthening descending inhibitory pathways of pain control

🚩Tapentadol is  seen  by some  as  similar  to tramadol,  but differs in a number of important points:

▶️It is not a racemic mixture of two enantiomers with different pharmacological effects

▶️Has  no  active  metabolites  (which  are  relevant  for tramadol’s mu opioid receptor agonism)

▶️Has only minimal serotonin effects

🚩This means that interactions with other serotonergic drugs (such as anti-depressants) are unlikely, reliance  on  metabolism  by  the  cytochrome  P450 system  for  increased  efficacy  is  not  required  and  retention of  active  metabolites  causing  potential  adverse  effects  is  not a concern.

NB

🔻Tramadol is a 4 phenyl piperidine analogue of codeine

🔻It has a weak central action at opioid receptors

🔻And also on descending monaminergic pathways (also responsible for the side effects)

🔻Hence known as an atypical centrally acting opioid

🔻It's M1 metabolite has more affinity to opioid receptors than parent compound

🔻So metabolites are important in maintaining efficacy

#Opioids , #Pharmacology , #analgesia , #PalliativeCare , #Pain , #SideEffects , #NewDrugs , #medicine , #anaesthesia

Reference: Recent advances in the pharmacological management of acute and chronic pain Stephan A. Schug, Catherine Goddard, Annals of Palliative Medicine, Vol 3, No 4 October 2014

Monday, January 9, 2017

NEURO #ANATOMY OF THE OLFACTORY SYSTEM : How some smells induce tears and sniffing in you❓

😤 Olfactory receptors1️⃣ are the most important cells of the olfactory epithelium and they are the first order neurons of the cranial nerve I

😤There are approximately 100 million such receptors in the olfactory epithelium found along the roof of the nasal cavity including the superior and upper middle conchae

😤Olfactory receptors project through the cribiform plate in the ethmoid bone

😤They have multiple cilia immersed in a surrounding matrix of mucus and a long dendrite

😤Odiferous chemicals get dissolved in this mucus and then trigger the olfactory receptors

😤The impulses pass through the neuron to the olfactory bulb (lies in base  of frontal  cortex in anterior  fossa), which has projections to cortical areas

😤The primary olfactory area in the temporal lobe process such informations through it's connections with the hypothalamus, thalamus and frontal cortex

😤The other major cell type is basal cells2️⃣ found deep to the olfactory neurons (olfactory neurons have a half-life of one month) and replace them, as they mature

😤3️⃣Sustentacular or supporting cells constitute the columnar mucus epithelium found between the receptors

😤There are 4️⃣Olfactory (Bowman’s) glands found in the connective tissue beneath the olfactory epithelium which produce the mucus in which the odiferous chemicals dissolve

❓➡️ 🅰️ Finally answer to the question

😤The innervation of the olfactory epithelial cells from cranial nerve VII (facial nerve) explains the tears and sniffing evoked by some smells.

Reference: Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology, 8th edn. New York, NY: HarperCollins, 1996; pp. 454–5

#smell , #Olfaction , #PhysiologyForExams , #NeuroAnatomy , #anesthesiology

Monday, January 2, 2017

♈️#PhysicsForAnesthesiologist : Beer-Lambert Law



☢️The #pulseoximeter works based on Beer-Lambert law, which relates the attenuation of light to the properties of the material through which the light is travelling. 


☢️It helps us in the calculation of the absorbance of a solution.


☢️According to the law, the absorbance of a solution depends on:


🖍The concentration of that solution, i.e. the more molecules of a light-absorbing compound there are in the sample, the more light will be absorbed. 


🖍The path-length of light travelling through the solution, i.e. the longer the length of the sample container, the more light will be absorbed because the light will come into contact with more molecules.


🖍A = εlc where 


🔻A is absorbance of light


🔻ε is the molar extinction coefficient(l mol–1 cm–1). It compensates for variance in concentration and the path-length, to allow comparison between solutions. 


🔻l is the length of solution that the light passes through. 


🔻c is the concentration of the compound in solution, expressed in mol L–1


☢️In the pulse oximeter, the concentration and molar extinction coefficient are constant. The only variable becomes the path length, which alters as arterial blood expands the vessels in a pulsatile fashion.


#Anesthesia, #PhysicsAndMedicine , #MedicalExams

Sunday, January 1, 2017

The science behind the pulse oximetry

☝️️Pulseoximeter measures the percentage of arterial hemoglobin in the blood that is saturated with oxygen
☝️️It consists of 2 LEDs & a photodiode arranged on either side of an adhesive strip and an electronic processor 
☝️️Light from LEDs travel through the patient's body part and is detected by the photodiode
☝️️One LED emits light at 660 nm (red light) and the other at 940 nm (infrared light). 
☝️️Oxyhaemoglobin and deoxyhaemoglobin absorb these wavelengths differently
☝️️Oxyhaemoglobin absorbs more infrared light (940 nm) and allows more red light (660 nm) to pass through. 
☝️️Deoxyhaemoglobin absorbs more red light (660 nm) and allows more infrared light (940 nm) to pass through.

☝️️Isobestic point is at 806 nm

☝️️The LEDs flash in sequence: one on, then the other, then both off (to allow correction for ambient light). This triplet sequence happens 30 times per second

☝️️The amount of light transmitted through the patient at each frequency is detected by the photodiode. 
☝️️The microprocessor corrects for ambient light, and also for the difference between arterial and venous saturations by deducting the minimum transmitted light, during diastole, from the maximum during systole.
☝️️After this, the ratio of oxy to deoxyhaemoglobin is determined and from this the percentage oxygen saturations is determined, using an empirical table derived from healthy volunteers who were exposed to varying degrees of hypoxia.
💅🏽Apart from the common causes like movement, nail varnish, diathermy,  others like 
🔻severe anaemia 

🔻cardiac arrhythmias 

🔻Methaemoglobinaemia (characteristically cause saturations to be measured at around 85%) 

🔻Increased venous pulsation, e.g. severe tricuspid regurgitation 

🔻i.v. methylene blue dye (because it absorbs light in the 660–670 nm range 
also may cause erroneously low readings)
💅🏻Carboxy hemoglobin (CO-Hb has similar absorption spectra as that of oxy-Hb) is detected by normal pulse oximeters as oxy hemoglobin--> erroneous high readings 
💅🏻Cyanide prevents oxygen being utilised in respiration and so its extraction from the blood falls; so in cyanide poisoning, though the value is not inaccurate, it should be interpreted as inappropriately high.
☝️️Fetal haemoglobin and Hb S (sickle) do not affect readings
☝️️The human volunteers used to construct empirical saturation tables did not have their oxygen saturations dropped below approximately 85%; hence readings below this number are extrapolated, not validated. 


Tuesday, December 27, 2016

A SORE STORY : THE PROPELLORS OF #INFLAMMATION



🔥The process of inflammation is maintained by 3 important mechanisms:

✔️Vasodilation 
✔️Increased capillary permeability 
✔️Migration of leucocytes

🔥WHO IS DOING THESE?

▪️PLASMA DERIVED MEDIATORS 

✔️BRADYKININ --> Vasodilation & Increased capillary permeability 

✔️COMPLEMENT MEDIATORS --> Mast cell degranulation --> Vasodilation & Increased capillary permeability + activate neutrophils and phagocyte migration 

✔️COAGULATION: Forms a protective clot over the injured area

✔️ FIBRINOLYSIS: Activates neutrophils & macrophages by Fibrin Degradation Products (FDP)

▪️CELL DERIVED MEDIATORS

✔️HISTAMINE (from basophils and mast cells) --> Vasodilation & Increased capillary permeability 

✔️LEUKOTRIENES (from basophils and mast cells) --> chemotaxis of granulocytes 

Ⓜ️NEMO> " leukoTRYenes TRY to catch granulocytes"

✔️TUMOR NECROSIS FACTOR (cytokine from macrophage) --> activates endothelial cells , enhances phagocytosis 

Ⓜ️NEMO> "TN(F)™ = F for 'Fagocytosis' TM= TNF is from Macrophages "

✔️CHEMOKINES are chemotactic #cytokines

✔️NITRIC OXIDE (from endothelial cells and macrophages) is a powerful vasodilator and smooth-muscle relaxant.

#anesthesia , #anaesthesia , #pathology , #exams , #MedicalStudents , #MedicalExams

Tuesday, December 20, 2016

The Life of P.I. (PERFUSION INDEX)🐾

🚤 Reduction of plethysmographic pulse wave amplitude (PPWA) has been proven to be a reliable method for detecting the IV injection of an exogenous vasopressor ( for e.g. The adrenaline in epidural test dose)


🚤 Currently, a numerical value has been added to new pulse

oximeters indicating the PPWA, termed the perfusion index (PI), to augment its clinical applicability.


🚤i.e. PI is the numerical value of the amplitude of the

plethysmographic pulse wave that is displayed on

many pulse oximeters.


🚤 Using pulse oximetry, a variable amount of light is absorbed by pulsating arterial flow (AC) and a constant amount of light is absorbed by nonpulsating blood and tissue

(DC). The pulsating signal indexed against nonpulsating signal and expressed as ratio is commonly referred to as the perfusion index


🚤 It depends on the distensibility of the vascular wall and the intravascular pulse pressure. Usually the effect of autonomic impulses upon distensibility is so strong that it predominates the opposite effect of pulse pressure.


🚤 Decreases in PI resulting from pain and other stressful stimuli are due to vasoconstriction of the finger arterial bed rather than changes in the pulse pressure


Reference: The Efficacy of Perfusion Index as an Indicator for Intravascular Injection of Epinephrine-Containing Epidural Test Dose in Propofol-Anesthetized Adults, Anesth Analg 2009;108:549 –53)