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

ANESTHESIA IMPLICATIONS IN MYESTHENIA GRAVIS

 

No priming/ precurarization with NMBA

Can cause airway obstruction during induction

Less efficacy of neostigmine as patient is on long term pyridostigmine

High risk of phase 2 block with succinyl choline

Sevoflurane better to use <1 mac; >1 MAC can produce significant NMB

In fact, we can avoid nmba fully with sevoflurane

Better to monitor tof even with sevo alone

Steroids reduce dose requirement of nmba

If pulmonary reserve is poor ...consider plasmapheresis

Whether to continue anticholinesterase, d/w neurologist

Regional anesthesia is better

PAIN CAN PRECIPITATE MYASTHENIC CRISIS: So give good postoperative analgesia

NIMODIPINE 🎯

 

ADMINISTRATION  ROUTES: 

PO,  IV

 ICU  INDICATIONS:

 1. Prophylaxis  and  treatment  of  cerebral  vasospasm  after  aneursymal  subarachnoid haemorrhage

 PRESENTATION AND ADMINISTRATION: IV: Nimotop  infusion  solution:  10mg  nimodipine  /  50ml 

Use  only  infusion  pumps  with  polyethylene  (PE)  infusion  tubing,  polypropylene  (PP) syringes  and  polyethylene  or  polypropylene  extensions,  taps  and  connectors.    Do  not use  polyvinylchloride  (PVC)  infusion  tubing  as  nimodipine  is  absorbed  by  the  tubing. Administer  nimodipine  neat.    Give  via  a  three-way  stopcock  with  a  coinfusion  of compatible  IV  fluid  in  a  ratio  of  1:4  (nimodipine:  coinfusion).    For  example,  an  infusion running  at  10ml/hr  requires  a  co-infusion  of  40ml/hr. Compatible  with  the  following  IV  fluids: 

Normal  saline   

5% dextrose    

Mannitol  10%   

5% albumin 

Hartmanns     

Protect  from  light.    Infusion  solution  is  light  sensitive.    Do  not  use  in  direct  sunlight. Note:  administration  of  nimodipine  via  a  central  line  is  preferred  as  nimodipine  causes thrombophlebitis  when  administered  peripherally.    If  necessary,  the  peripheral  route  can be  used  (although  administration  via  this  route  is  not  licensed)

 PO: Nimotop  tablets  30mg  (yellow) 

DOSAGE: IV: Commence  infusion  at  1mg/hr  (5ml/hr)  for  two  hours  and  then  increase  to  2mg/hr  (10ml/ hr)  if  tolerated.    For  patients  who  are  unable  to  tolerate  infusion  at  1mg/hr,  commence infusion  at  0.5mg/hr  (2.5ml/hr) 

Weaning  from  IV  to  oral  therapy: Commence  regular  oral  therapy  (see  below).    After  the  first  dose  of  nimodipine  is  given, reduce  infusion  by  1  mL  every  hour  for  5  hours,  then  cease  infusion.    If  the  patient becomes  hypotensive  after  oral  nimodipine  is  given,  cease  the  infusion  immediately. Observe  for  neurological  deterioration.    If  the  patient  does  deteriorate  neurologically, cease  weaning  off  IV  nimodipine  and  return  to  full  IV  therapy. 

PO: 60mg  4  hourly  for  21  days;  if  not  tolerated  due  to  hypotension,  try  a  reduced  dose  of 30mg  4  hourly. 

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

DOSAGE  IN  PAEDIATRICS: 10-15mcg/kg/hr  IV  for  2  hours  then  10-45mcg/kg/hr

CLINICAL  PHARMACOLOGY: Nimodipine  is  a  calcium  channel  blocker 

 CONTRAINDICATIONS: 1. Hypersensitivity  to  nimodipine Nimodipine WARNINGS Nimodipine  can  cause  hypotension.    If  hypertensive  therapy  is  being  pursued  or  the patient  develops  significant  hypotension  during  nimodipine  treatment,  the  dose  should be  reduced  or  nimodipine  should  be  withheld. 

PRECAUTIONS General The  metabolism  of  nimodipine  is  decreased  in  patients  with  impaired  hepatic  function. Such  patients  should  have  their  blood  pressure  and  pulse  rate  monitored  closely  and should  be  given  a  lower  dose.    (usually  50%  of  normal  dose) 

IMPORTANT  DRUG  INTERACTIONS  FOR THE  ICU: The  risk  of  hypotension  increases  with  concomitant  administration  of  other antihypertensive  drugs.

ADVERSE  REACTIONS 

Hypotension,  tachycardia,  bradycardia, deranged  liver  function  tests,  diarrhoea, Headache

FOSPROPOFOL DISODIUM

Fospropofol  is a watersoluble prodrug of propofol that results in incomplete (20–30%) liberation of propofol into the systemic circulation by alkaline phosphatase. It is believed that most (70–80%) of the propofol liberated is further metabo-lized prior to entering the systemic circulation. The peak hypnotic effect occurs approximately 10 minutes following a bolus injection. The kinetic disposition of liberated propofol differs from that of an injected propofol emul-sion, with the former being slower for reasons that remain unexplained.

Apparent advantages of an aqueous solution of fospropofol are a reduced risk of bacterial contamination com-pared with a propofol emulsion and the absence of an infused lipid load that has been associated with organ toxicity during long-term infusions of a propofol emulsion. Whether the new medication will cause less pain on injection remains to be determined. The relatively slow-onset kinetics of fospropofol probably would not make it useful for induction of general anesthesia. It may find utility for sedation in the ICU, procedural sedation outside of the operating room (where its safety needs to be demonstrated), and for sedation during monitored anesthesia care or regional anesthesia during which a rapid onset is less critical.

ACETAZOLAMIDE (Diamox)

 INDICATIONS: 1. Diuretic  (particularly  in  the  presence  of  metabolic  alkalosis) 2. Correction  of  severe  metabolic  alkalosis

Diamox  250mg  tablets  

 DOSAGE: For  diuresis,  the  dose  is  usually  250-375  mg  stat.  If,  after  an  initial  response,  the  patient fails  to  continue  to  diurese,  do  not  increase  the  dose  but  allow  for  kidney  recovery  by skipping  medication  for  a  day.  Acetazolamide  yields  best  diuretic  results  when  given  on alternate  days,  or  for  2  days  alternating  with  a  day  of  rest. 

DOSAGE  IN  PAEDIATRICS: The  safety  and  effectiveness  of  acetazolamide  in  paediatric  patients  below  the  age  of 12  years  have  not  been  established. 

DOSAGE  IN  RENAL FAILURE AND  RENAL REPLACEMENT THERAPY: No  dose  adjustment  is  required  when  administered  for  ICU  indications  (beware  that acetazolamide  is  contraindicated  in  the  presence  of  metabolic  acidosis). This  drug  is  not  indicated  in  patients  on  renal  replacement  therapy.   

CLINICAL  PHARMACOLOGY Acetazolamide  is  an  enzyme  inhibitor  that  acts  on  carbonic  anhydrase,  the  enzyme  that catalyzes  the  reversible  reaction  involving  the  hydration  of  carbon  dioxide  and  the dehydration  of  carbonic  acid.

 CONTRAINDICATIONS 1. Hypersensitivity  to  acetazolamide  or  other  sulphonamides 2. Metabolic  acidosis 3. Cirrhosis  (risk  of  development  of  hepatic  encephalopathy) 

General Increasing  the  dose  does  not  increase  the  diuresis  and  may  increase  the  incidence  of drowsiness  and/or  paraesthesia.  Increasing  the  dose  often  results  in  a  decrease  in diuresis. 

Acetazolamide  and  sodium  bicarbonate  used  concurrently  increases  the  risk  of  renal calculus  formation.

METABOLIC SIDE EFFECTS 

Metabolic  acidosis,  electrolyte  imbalance,  including  hypokalaemia,  hyponatraemia,  loss of  appetite,  taste  alteration,  hyper/hypoglycaemia.

ECG CHANGES IN SAH

🚩Deep T wave inversions. 

🚩Prolonged QT.

🚩Tall R waves. 

🚩ST depression

🚩Large U waves

🚩 ST elevations that seem to resolve while ‘T’ wave inversions appear to persist—even for months/years

〰〰〰〰〰〰〰〰

DO YOU KNOW?

ASA-2014 UPDATE

A social drinker is ASA II

A smoker is ASA II

Pregnant patient is ASA II

Obese patient is ASA II

Morbid obesity is not ASA II, but ASA III

Alcohol dependence without any documented systemic illness is also ASA III

Premature infant is ASA III

ESRD with regular HD is ASA III

ESRD without regular HD is ASA IV

Evidence of Sepsis or DIC- ASA IV

Intracranial bleed with mass effect is ASA V

A cardiac patient with bowel ischemia is ASA V