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

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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

VISUAL IMPAIRMENT INTRACRANIAL PRESSURE SYNDROME & OCT

Visual acuity degradation in astronauts exposed to microgravity is a newly recognized phenomenon. Prompted by persistent reports of vision changes, NASA began a stepwise operational process to determine the cause 

        although  the exact mechanism is yet to be fully determined, many MRI findings suggest that intracranial hypertension is an important component. 

  

       OCT ( Optical Coherence Tomography ) is one technology that is operational @NASA's International Space Station, to study this Visual impairment Intracranial Pressure Syndrome. It is useful to analyse pathologies in the context of raised ICP. It can assess the Retinal Nerve Fibre Layer ( RNFL), total retinal thickness and the optic nerve head volume. But it can't provide a direct indication of raised ICP, is bulky, expensive and need an external energy source.

J Neurosurg Anesthesiol 27/4 Oct/2015

SPONDYLOEPIPHYSEAL DYSPLASIA

ANESTHETIC CONCERNS

1. Short trachea with 15 rings or less; high chance of accidental one lung ventilation

2. Chances of Laryngeal Stenosis... Some times an unanticipated difficulty for passing tube, may trigger edema and stridor ( one such case reported, needed emergency tracheostomy)

3. Atlanto axial instability, can cause, massive cord edema, even with moderate neck flexion ( one case suffered tetraparesis after intubation; so in clear words, explain to the relatives..,the anticipated amount of morbidity and mortality) Take LATERAL CERVICAL SPINE VIEWS IN FLEXION AND EXTENSION PREOPERATIVELY. If atlantoaxial instability is present and patient requires GA, give MANUAL IN LINE STABILIZATION/ do AWAKE FOB.

4. Restricted lung function accompanied by impending respiratory failure, is a situation, where we may be more inclined towards SAB in such patients (e.g. Pregnancy, where the uterus further compromise lung function).  So regional anesthesia may be appropriate, if technically feasible.

5. Technical difficulties with SAB/EDB; epidural space located 2.5 cm from skin was reported in one case.

KNOWN SECRETS! - COEXISTING ILLNESS AND ANESTHESIA

1. The evaluation of risk factors,  is for planning the anesthetic management, and will be of no use in predicting the outcome.
2. There is no justification for performing revascularisation purely to facilitate elective non cardiac surgery.
3. M.I. within the last 6 weeks, class iii-iv angina, decompensated heart failure, malignant arrhythmias, severe valvular heart disease, CABG/PTCA within the last 6 weeks constitute major Cardio Vascular risk factors for surgery.
4. Previous M.I. (>6weeks), class i-ii angina, compensated heart failure, T2 DM constitute intermediate C. V. risk factors.
5. Age > 70 years, uncontrolled systemic hypertension, arrhythmias, family h/o CAD, dyslipidemia, smoking, renal dysfunction, ECG abnormalities (LVH, RBBB/LBBB, ST segment anomalies) constitute minor C. V. risk factors.
6. Only emergency, life saving procedures should be performed during the first 6 weeks after a myocardial infarction (M. I.) and after CABG/PTCA with or without a coronary stent. The period between 6 weeks and 3 months are considered as a period of intermediate risk,  when non urgent elective surgery should be postponed.
7. SURGICAL PREDICTORS OF INCREASED PERIOPERATIVE CARDIOVASCULAR RISK
(i) HIGH RISK (complication rate >5%)
#Emergency major to intermediate surgery, especially in elderly patients
#Aortic & major and also peripheral vascular surgery
#Procedures involving: hem
dynamic instability, long duration or large fluid/blood loss
(ii) INTERMEDIATE RISK (complication rate 1-5%)
#Carotid endarterectomy
#Head & neck surgery
#Abdominal/thoracic surgery
#Orthopaedic surgery
#Prostatectomy
(iii)LOW RISK (complication rate <1%)
#Endoscopic procedure
#Breast and superficial surgery
#Eye surgery
8. ACE inhibitors are withheld for 24 hours by some anesthetists.
9. Perioperative beta blockade should be continued for 72 hours postoperatively.
10. The gold standard for detecting intraoperative ischemia and assessing volume status & valvular function is TEE.
11. Most perioperative myocardial infarctions occur in the first 3 days postoperatively. Patients at risk for M.I. require effective analgesia and humidified oxygen therapy for atleast 72 hours after major surgery.
12.  Severe hypertension (grade 3) has been associated with an increased incidence of perioperative hemodynamic instability, silent m.i. and arrhythmias; but evidence of a clinically significant increase in adverse outcome is lacking. The presence of endorgan damage due to hypertension is more important than the blood pressure per se.
13. Ideally the blood pressure should be maintained within 20% of the best estimate of preoperative pressure.
14. The treatment of arrhythmias produced by WPW syndrome includes Flecainide, Disopyramide, Procainamide and Amiodarone. Dgoxin and Verapamil are contraindicated.
15. There is no evidence to suggest that, frequent ventricular ectopics or asymptomatic non sustained ventricuar tachycardia is associated with an increased incidence of perioperative m.i..
16. Sick sinus syndrome is associated with a high ris of thromboemboism and may be anticoaguated. If the patient is not having a permanent pacemaker, he/she needs a, temporary pacing wire inserted preoperatively.
17. Complete heart block, type ii second degree A-V block and lesser degrees of heart block, in the presence of symptoms or cardiac failure requires preoperative insertion of permanent or temporary insertion of pacemaker. Vlatile agents prolong cardiac conduction and can worsen heart block. Atropine, Isoprenaline and facilities for external pacing should be kept ready.
18. ATRIOVENTRICULAR BLOCKS
(i) First degree block: P-R interval > 0.2 sec
(ii)Second degree block
Type I: progressive lengthening of PR interval,  until conduction fails and a beat is dropped.
Type II: intermittent failure of AV conduction without preceding PR prolongation.
(iii) Third degree block
Complete dissociation of atria and ventricles as atrial impulses fails to be transmitted. 
19. CHECKLIST FOR A PATIENT WITH PACEMAKER
a. Indication for pacemaker insertion
b. Mode of function of pacemaker
c. Functional status
d. Consider conversion of rate responsive pacemakers to fixed rate in the perioperative period.
e. Ensure use of only bipolar diathermy
f. If unipolar diathermy must be used, then the ground plate should be placed on the same site as the operating site, as far away from the pacemaker as possible. The frequency and duration of use should be minimised and the lowest possible current used.
g. MRI is contraindicated
h. Magnets should not be placed over pacemakers during surgery,  as they have an unpredictable effect on the programming of modern pacemakers.
i. A backup pacing system, atropine, adrenaline, isoprenaline and a backup pacing system should be available, in case of pacemaker failure.
20. Anesthesia constitutes a significant risk in Hypertrophic Obstructive Cardiomyopathy. Patients will be having dynamic left ventricular outflow tract obstruction, often with secondary MR. They are prone to arrhythmias and sudden cardiac death. Look for an Ejection systolic murmur in auscultation and LVH in ecg. Confirmation is by ECHO. Avoid hypovolemia, vasodilatation and the use of catecholamines
21. Constrictive pericarditis poorly tolerate vasodilatation; especially at induction.
22. In valvular heart disease, antibiotic prophylaxis is especially required for dental surgeries and those involving instrumentation of upper respiratory tract and genitourinary system.
23. AORTIC STENOSIS
# Even an ejection systolic murmur in an asymptomatic patient also warrants careful preoperative examination/ ECHO, as symptoms tend to appear late in the disease only.
# Promptly treat tachycardia and AF.
# Maintain ventricular filling by avoiding hypovolemia and maintaining SVR.
# Vasodilatation may result in profound hypotension--> subendocardial ischemia and even sudden death.
# Aggressive treatment of hypotension is mandatory to prevent cardiogenic shock and/or cardiac arrest. Cardiopulmonary resuscitation is unlikely to be effective in patients with aortic stenosis because it is difficult, if not impossible, to create an adequate stroke volume across a stenotic aortic valve with cardiac compression.
24. AORTIC REGURGITATION
# Avoid vasoconstriction and bradycardia which increases the degree of regurgitation
# A mild tachycardia, moderate fluid loading, a degree of vasodilatation and avoidence of myocardial depression can improve the forward flow.
# Acute AR is a surgical emergency and may respond poorly to vasodilatation.
25. MITRAL STENOSIS
# Patients are prone to develop CCF and Pulmonary Edema.
# Atrial fibrillation is a trigger for acute deterioration; so should be treated preoperatively
# Avoid tachycardia, myocardial depression and excessive vasodilatation
# Hypovolemia compromises ventricular filling
# Fluid overload can easily precipitate pulmonary edema
# PCWP will be inaccurate in the presence of pulmonary hyperension. Avoid Nitrous oxide if there is evidence of pulmonary hypertension.
26. MITRAL REGURGITATION
# A mild tachycardia,  a slight reduction in SVR and avoidance of myocardial depression are desirable.
# Avoid hypovolemia
27. There is little evidence that GA in ADULTS with URTI is associated with an increased risk of adverse respiratory events, although upper airway reactivity may be increased
28. In children with URTI,  a higher incidence of adverse respiratory events have been demonstrated,  but few of these adverse events result in postoperative sequelae. It has been suggested that surgery need not necessarily be postponed in children with mild URTI. Increased airway reactivity may persist for 4-6 weeks and if surgery is postponed, it should be for a period of at least 6 weeks.
29. In COPD, if the patient is having copious secretions, better to avoid anticholinergics, as it will impair the ability to clear secretions.
30. Even though regional anesthesia has the advantage of avoiding respiratory complications of GA, most patients, even those with quite severe COPD may be managed safely under carefully c
ducted GA.
31. Pressure Controlled Ventilation with a low respiratory rate and prolonged expiratory phase is suitable in COPD patients.
32. Epidural analgesia has been shown to decrease the incidence of postoperative pulmonary complications in thoracic and upper abdomnal surgery.
33. In patients with bronchial asthma, good depth of anesthesia, good muscle relaxation and i. v.  Lidocaine can reduce the incidence of bronchospasm during intubation; topical lidocaine spray is not effective and may induce bronchoconstriction in some patients.
34. Circulatory disturbance during anesthesia and surgery may affect the absorption of subcutaneous insulin.

ANESTHETIC MANAGEMENT OF PATIENT, WITH HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

Tachycardias from emotion, exercise and pain, and drugs such as digoxin and beta stimulators, will all increase the outflow tract gradients and may considerably reduce the cardiac output to essential organs, such as the myocardium and brain.Preoperative beta blockers should be maintained.(Patients are often already taking beta blockers to prevent tachycardias.)

Hypotension from blood loss, regional anaesthesia, or vasodilator drugs, cause similar reductions in cardiac output and can worsen obstruction.Drugs and techniques that cause vasodilatation and hypotension must be avoided,contraindicated. However, with the greater ability to control the onset of epidural and by the use of continuous infusions and opiates, it has been suggested that regional blocks are no longer contraindicated. Hypotension should be treated by restoring vascular volume. If vasopressors are required, an alpha1agonist, such as phenylephrine or methoxamine, is the most suitable.

An adequate preload should be given and blood loss should be replaced promptly.