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Tuesday, December 8, 2015

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

Monday, December 7, 2015

👁➖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 
➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖

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

Saturday, December 5, 2015

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

Tuesday, December 1, 2015

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

Monday, November 30, 2015

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

Sunday, November 29, 2015

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

Saturday, November 28, 2015

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

Thursday, November 26, 2015

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

Wednesday, November 25, 2015

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.



Tuesday, November 24, 2015

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)