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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)

Saturday, November 21, 2015

❗️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

Friday, November 20, 2015

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

Thursday, November 19, 2015

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. 


Tuesday, November 17, 2015

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

Monday, November 16, 2015

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

Sunday, November 15, 2015

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)