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Friday, August 19, 2016

HOW EVOKED POTENTIALS BEHAVE , WHEN BRAIN SUFFERS FROM ISCHEMIA ❓


🕶Cerebral ischemia slows neurotransmission and neuronal energy metabolism, resulting in decreased amplitude and increased latency of specific peaks. 

🕶For SSEPs, a 50% reduction in amplitude and/or a 10% increase in latency [changes in the central conduction times, namely, the interpeak latencies between the N14 and N20 peaks] of SSEP signals from the baseline are generally accepted to be a significant change 

🕶A 50% reduction on SEP amplitude has been shown to occur when cerebral blood flow decreases below 14 mL/100 g/min 

🕶MEP have less well-defined warning criteria as compared to SSEPs; however, increased stimulus thresholds and/or decreased MEP amplitudes in relation to dramatic events (i.e., clip application) are indicative of pending neurologic insult. 

🕶For BAEP, an increase in latency of more than 1 msec, particularly in wave V, is considered to be clinically significant. 

🕶Unlike EEG monitoring the evoked potential tests can detect subcortical functional status by way of perforating branches such as the anterior choroidal and medial striate arteries 

Reference: Anesthesiology Research and Practice Volume 2014, Article ID 595837, Controversies in the Anesthetic Management of Intraoperative Rupture of Intracranial Aneurysm, Tumul Chowdhury, Andrea Petropolis,Marshall Wilkinson, Bernhard Schaller  Nora Sandu and Ronald B. Cappellani

ADENOSINE INDUCED TRANSIENT ASYSTOLE FOR INTRACRANIAL ANEURYSM CLIPPING SURGERY


▶️Adenosine alters electrical conduction at the atrioventricular (AV) node and has a negative chronotropic effect on the sinoatrial node. 

▶️Adenosine acts on cardiac A1 receptors to reduce cAMP activity, which decreases inward calcium conductance and diminishes pacemaker current, resulting in bradycardia, AV nodal blockade, and sinus pauses. 

▶️It has a very short half-life time (less than 10 seconds) and is rapidly taken up by the vascular endothelium and erythrocytes. 

▶️The effect on heart rate is seen within 10 to 20 seconds after administration

▶️ There is a relative hypotension period, 1 minute after asystole

▶️Multiple doses are usually required for very large and complex aneurysms to obtain repeated episodes of asystole

▶️ Bebawy et al. recommended an initial dose of between 0.3 and 0.4 mg/kg ideal body weight (IBW) 

▶️ Powers et al. gave a standard 6 mg dose initially escalated to 6 mg more than the previous dose (e.g. 6 mg, 12 mg, 18 mg, 24 mg ; repeating the dose as often as every 1 to 2 minutes) until 30 to 40 seconds of asystole was reached.

▶️ Guinn NR et al reported the median dose of intravenous adenosine resulting in bradycardia greater than 30 seconds was 30 mg. The median dose of adenosine resulting in hypotension greater than 30 seconds was 15 mg, and greater than 60 seconds was 30 mg

▶️Luostarien et al. reported that the median dose for a single bolus was 12 (6–18) mg, whereas the median total dose for multiple boluses was 27 (18–89) mg

▶️ Hypotension ( most often transient , sometimes requiring vasopressors), atrial fibrillation etc were reported as side effects 

▶️ Adenosine-induced flow arrest briefly reduces cerebral perfusion pressure and reduces the turgor of the aneurysm, thereby facilitating the clip ligation 

▶️ The adenosine dose will achieve approximately 45 seconds of controlled systemic hypotension and a bloodless surgical field.

▶️ Periods of flow arrest have to be carefully coordinated with the surgeon such that necessary working time is available for aneurysm dissection and clip placement

Reference: Adenosine-Induced Transient Asystole
Gavin W. Britz, Methodist Debakey Cardiovasc J. 2014 
Oct-Dec; 10(4): 220–223.

Adenosine-induced transient asystole for intracranial aneurysm surgery: a retrospective review. Guinn NR, et al. J Neurosurg Anesthesiol. 2011.

Wednesday, August 17, 2016

DRAW-OVER VAPORISERS IN A NUTSHELL FOR EXAMS


🏺They are placed inside the breathing system and rely on a negative pressure downstream from the vaporiser to create the flow required to entrain the agent. This negative pressure is generated either by the patient’s own inspiration or by a self-inflating bag

🏺So they must have a very low resistance to flow to avoid additional resistance to the patient’s breathing. 

🏺Goldman vaporiser, the Oxford miniature vaporiser (OMV) and the Epstein MacIntosh vaporiser (EMV) etc are draw-over vaporisers. The triservice apparatus, used by the military, incorporates two OMVs

🏺 They are simpler, lightweight, smaller and less expensive. 

🏺 As it is not possible to calibrate for the large range of tidal volumes created by the patient/ self-inflating bag, they are inaccurate 

🏺So they are not generally used in hospitals, and are reserved for ‘in-the-field’ use, where portability is required. 

Reference: Al-Shaikh B, Stacey S. Essentials of Anaesthetic Equipment, 2nd edn. Edinburgh: Churchill Livingstone, 2002 . Davis PD, Kenny GNC. Basic Physics and Measurement in Anaesthesia, 5th edn. Oxford: Butterworth–Heinemann, 2003 .

Sunday, August 14, 2016

Physics For Anesthesiologist ( #PFA ) : #IMPEDANCE


🖊Impedance is a term that is commonly used in the world of #electrophysiology and #BiomechanicalEngineering. 

🖊The chance of getting an electric shock is high when you have wet hands because the impedance of the skin is lower than when it is dry. 

🖊Thoracic impedance increases during inspiration.

🖊When applying electric current to the chest during #defibrillation, less energy may reach the heart during the inspiratory phase than during the expiratory phase because of this phenomenon, thereby decreasing the possible success of defibrillation. 

🖊So better to attempt defibrillation during the expiratory phase of mechanical ventilation.

🖊Where the #resistance of a circuit is dependent on the frequency of the current through it, the term impedance is used. 

 🖊The unit of impedance is therefore the same as that of resistance (the ohm), but the symbol Z is used to differentiate it from the symbol used for resistance (Ω).

🖊In case of a capacitor, as the frequency of the current increases, the current passes through the circuit more easily, i.e. the resistance of the capacitor falls with increasing current frequency. 

🖊In contrast, the resistance of an inductor rises as the frequency of the current increases.

#PhysicsForAnesthesiologist , #anesthesiologist , #anesthesia , #biomedical

Davis PD, Kenny GNC. Basic Physics and Measurement in Anaesthesia, 5th edn. Oxford: Butterworth–Heinemann, 2003; pp. 149–64 . Ewy GA, Hellman DA, McClung S, Taren D. Influence of ventilation phase on transthoracic impedance and defibrillation effectiveness. Crit Care Med 1980; 8: 164–6

Saturday, August 13, 2016

LESSER KNOWN FACTS ABOUT A WELL KNOWN PERSON : PROPOFOL



✔️Pain on injection due to Propofol is INCREASED BY

🔹rapid injection

🔹lower temperature of the propofol 

🔹the use of an IV carrier infusion to dilute the propofol as it enters the vein

✔️ Propofol is almost entirely un-ionised in solution

✔️ The soya bean oil and egg components are denatured by processing and there is no evidence that propofol should be avoided in patients with allergies to eggs or soya

Reference: Pandit J. Intravenous anaesthetic agents. Anaesth Intens Care Med 2007; 9 (4): 154–9 

#Propofol , #EggAllergy , #anesthesia

Wednesday, August 10, 2016

A FEW CLINICAL SCENARIOS IN WHICH ECHOCARDIOGRAPHY CAN HELP THE #Anesthesiologist SIGNIFICANTLY IN THE CARE OF PATIENTS COMING FOR NON-CARDIAC SURGERIES


👁 During Pre Anesthetic Evaluation, to rule out structural heart disease. For e.g. A recent study identified a 12% incidence of moderate to severe aortic stenosis in unselected fractured neck of femur patients.

👁 When the nature of the planned surgery might result in severe haemodynamic, pulmonary or neurological compromise e.g. Neurosurgical procedures in the semi-sitting position, liver transplantation, scoliosis surgery, endovascular aortic stent graft placement and resection of renal tumours that extend into the inferior vena cava

👁 When the patient’s known or suspected cardiovascular pathology might result in severe haemodynamic, pulmonary or neurological compromise e.g. patients with dynamic outflow tract obstruction secondary to hypertrophic cardiomyopathy and those with ventricular assist devices in place.

👁Trans Esophageal Echo (TEE) can assess the volume status intraoperatively

👁  Persistent unexplained hypotension : Causes can be LV systolic or RV dysfunction, severe MR , dynamic LV outflow obstruction, cardiac tamponade , aortic dissection ( TEE is the technique of choice) , large pleural effusion etc

👁 Persistent unexplained hypoxaemia : A Patent Foramen Ovale can cause this

Reference: AAGBI Core Topics in Anaesthesia 2015 , Echocardiography and Anaesthesia, Jonathan H. Rosser and Nicholas J. Morgan-Hughes

Tuesday, August 9, 2016

HAVE YOU SEEN PERSISTENT UNEXPLAINED HYPOXAEMIA IN ADULT PATIENTS ❓ ONE IMPORTANT D.D. IS PFO❗️


▪️Persistent unexplained hypoxaemia can result from the presence of a Patent Foramen Ovale (PFO)

▪️A quarter of young adults have a #PFO

▪️Actually there is no deficiency of atrial septal tissue per se, in such cases

▪️In the absence of left atrial dilation, the defect functions as a flap valve, only allowing right-to-left flow. 

▪️Normally, left atrial pressure exceeds right atrial pressure and no shunting occurs. 

▪️ However, if right-sided pressures increase, right-to-left shunting and therefore potential hypoxaemia can occur. 

▪️ Acutely, this may become evident in such patients 

✔️during #ventilator asynchrony 

✔️with maintenance of high positive end-expiratory pressures (PEEP) during mechanical ventilation   

✔️in #ARDS patients with acute cor pulmonale or with right ventricular systolic dysfunction, particularly as part of the right ventricular infarction syndrome. 

▪️The diagnosis should be considered in any intensive care patient in whom the degree of hypoxaemia appears disproportionate, and should be detectable by colour Doppler. 

▪️Management might include a counterintuitive decrease in positive end-expiratory pressure ( #PEEP ) and the re-establishment of spontaneous ventilation.

Reference: AAGBI Core Topics in Anaesthesia 2015 , Echocardiography and Anaesthesia, Jonathan H. Rosser and Nicholas J. Morgan-Hughes

Friday, August 5, 2016

CAUSES OF DETERIORATION OF #GCS IN #NEUROSURGICAL #ICU



☑️IN A PATIENT WITH ANEURYSMAL-SAH, AFTER CLIPPING OR COILING 

❓Re-bleed 
❓Acute hydrocephalus 
❓Cerebral vasospasm 
❓Seizure

☑️ IN A PATIENT WITH TRAUMATIC BRAIN INJURY (#TBI)

❓Re-accumulation of haematoma 
❓ Haemorrhage into contusion 
❓ Oedema 
❓ Seizure

☑️IN A PATIENT, WHO UNDERWENT #CRANIOTOMY

❓ Haematoma (sub-dural/intracerebral etc.) 
❓ Oedema 
❓ Seizure 
❓ Pneumocephalus/ Air Encephalocoele

#NeuroAnesthesia , #NeuroCriticalCare , #NeuroIntensiveCare , #NeuroICU , #Anaesthesiology , #Anesthesiologist , #Anesthesia , #CriticalCare

Thursday, August 4, 2016

#Brainstem Testing for diagnosis of #BrainDeath


➖The brain stem often fails from the rostral to caudal direction and therefore it is logical to undertake testing in the same manner.


▶️PUPILLARY REFLEXES : 

➖The pupillary light reflex involves cranial nerves II and III and localizes to midbrain. The pupils should be nonreactive to both direct and consensual light reflex. 

POINTS: 

➖Pinpoint pupils are indicative of damage to descending sympathetic fibers as a result of damage to pons. 

➖The size of the pupils only provides an indication of the site of brainstem involvement and is not crucial for testing brain stem death.

▶️OCULOCEPHALIC REFLEX :

➖It involves cranial nerves III, VI, and VIII and interneurons within the midbrain and pons. On head movement toward right or left, the eyes remain “fixed” on a point in an intact patient. In the brain-dead patient, the eyes move with the head, hence the name “dolls eye” reflex.

POINTS: 

➖Before performing this test the physician must rule out cervical fracture or instability. 

▶️CORNEAL REFLEX : 

➖The reflex tests the V, VII, and III cranial nerves and localizes entirely to the pons. In the intact patient, touching the cornea with a cotton swab causes eyelid closure. 

➖The eye rotates upward, demonstrating the cranial nerve III component, known as “bell’s phenomenon.”

▶️OCULOVESTIBULAR REFLEX :

 ➖The oculovestibular reflex tests cranial nerves III, VI, VIII, and IV. It involves the entire pons and midbrain. 

PROCEDURE : 

➖Elevate the head 30°C. Irrigate tympanic membrane with 50-cc iced water or saline. Wait 1 min for response. Repeat test on the other side after waiting 5 min. If the oculovestibular reflex is intact using cold water as stimulus, the eyes tonically deviate toward the side of the stimulus immediately followed by a fast recoil toward the contralateral side (apparent nystagmus). In the brain stem dead patient this response is absent.

▶️GAG AND COUGH REFLEXES :

 ➖They require a functioning medulla and test cranial nerves IX and X. Both reflexes should be absent in brain stem death. 

➖The cough reflex is easily tested by stimulation of carina by suction through the endotracheal tube. The gag reflex can be elicited by stimulating the posterior pharynx with a tongue blade. 

▶️APNEA TESTING : 

➖This final test aims to demonstrate the failure of medullary centers to drive ventilation. Apnea test should be the last brain stem reflex to be tested. 

OBJECTIVE:  

➖is to stimulate the medulla while avoiding hypoxia and hemodynamic compromise associated with acidosis secondary to hypercarbia. 

PROCEDURE: 

➖After ensuring preoxygenation for 10 min a blood gas is performed to confirm baseline PaCO2 and SaO2 . 

➖With oxygen saturation greater than 95% the ventilatior is disconnected inducing apnea for a period of time to achieve ETCO2 above 6 KPa (=45 mmHg). A repeat arterial blood gases is used to confirm that the PaCO2 is at least 6 KPa and the pH is less than 7.40. 

➖An oxygen flow rate of 2–5 L/min via an endotracheal catheter or in difficult cases CPAP may be used to maintain oxygenation till this state is attained. 

➖Apnea is continued for a further 5 min after a PaCO2 of 6 KPa (=45 mmHg) has been achieved. 

➖If there is no spontaneous respiratory response, a presumption of absence of respiratory activity is made. 

➖A further blood gas can be done to confirm that the PaCO2 has risen by 0.5 KPa (=4 mmHg) from the initial 45 mmHg baseline.

Reference: Brain Death in Neurosurgical Critical Care Amit Prakash,  Basil Matta , Essentials of Neurosurgical Anesthesia & Critical Care 2012

Wednesday, August 3, 2016

UPPER GI BLEED IN ICU PATIENTS: THE POINTS WHICH YOU SHOULD KEEP IN MIND

💥Incidence of overt Upper GI Bleed (UGIB) ranges from 1.5 to 8.5% of all ICU patients but may be as high as 15% if no prophylaxis is used.

💥RISK FACTORS 

☢Mechanical ventilation >48 h 

☢Coagulopathy – INR >1.5 or platelet count <50,000 

☢Others: ✔️ Shock ✔️Sepsis ✔️Hepatic failure ✔️Acute Renal failure ✔️Multiple trauma ✔️Burns >35% of total body surface area ✔️Organ transplantation ✔️Head trauma ✔️Spinal trauma ✔️History of PUD or UGIB

💥SPECIFIC POINTS REGARDING TREATMENT 

🔸Thrombocytopenia can develop in neurosurgical patients on H2 Blockers

🔸The use of H2Bs and PPIs may increase the frequency of nosocomial pneumonia.

💥PROPHYLAXIS IS RECOMMENDED FOR ICU PATIENTS WHO EXHIBIT:

🔸Coagulopathy (platelet count < 50,000 per m 3 , INR > 1.5, partial thromboplastin time (PTT) >2 times the control value) 

🔸Mechanical ventilation >48 h 

🔸History of GI ulceration or bleeding within the past year 

🔸Two or more of the following risk factors: sepsis; ICU stay >1 week; occult GIB ≥6 days; glucocorticoid therapy (>250 mg hydrocortisone).


💥REASONS FOR UGIB IN ICU PATIENTS: 

🔸The glycoprotein mucous layer may be denuded by increased concentrations of refluxed bile salts or uremic toxins common in critically ill. Alternatively, or in addition, mucosal integrity may be compromised due to poor perfusion associated with shock, sepsis, and trauma. 

🔸Excessive gastrin stimulation of parietal cells has been detected in patients with head trauma as oppose to be normal or subnormal in most other ICU patients.

🔸Systemic steroids double the risk of a new episode of UGIB or perforation. Concomitant use with high doses of NSAIDs has been associated with a 12-fold increased risk for upper GI complications.

🔸Helicobacter pylori infection 

💥EMPIRICAL THERAPY

⚛ Start with an IV bolus of 80 mg and continue IV infusion at 8 mg/h for a total of 72 h. If no signs of rebleeding after 24 h, switch to oral PPI. 

⚛Octreotide is used in variceal bleeding. Start with an IV bolus of 50 mcg and continue IV infusion at 50 mcg/h for 3–5 days.

💥 UGIB IN HEAD INJURY & OTHER NEUROSURGICAL PATIENTS:

🔸They are more prone for UGIB because of ✔️ Frequent use of systemic steroids ✔️ Increased gastrin secretion ✔️ Significant gastric intramucosal acidosis is common in severe head injury. ✔️Primary insult to the central nervous system may result in derangement of splanchnic blood flow secondary to neurohumoral mechanisms.

🔸 In head injury, GI dysfunction also may manifest as ✔️gastroparesis✔️ileus, ✔️increased intestinal mucosal permeability, 

🔸 Plasma levels of cortisol and age are independent predictors of stress ulcers following acute head injury.

Reference: Gastrointestinal Hemorrhage in Neurosurgical Critical Care Meghan Bost, Kamila Vagnerova  , Ch:84, Essentials of Neurosurgical Anesthesia & Critical Care 2012 Strategies for Prevention, Early Detection, and Successful Management of Perioperative Complications