DISCLAIMER

The contents of this blog are solely meant for information & education purpose only.These may be the basis of actual treatment, but not necessarily. Information from other websites and journals are also included. So the author is not responsible for any inaccuracy,loss, or damage that may arise due to the use of these informations published here. I do respect copyright & always give credits to the original author(s) and thankful to them. Inspite of my utmost effort and care there can be human error. If anyone finds any violation of copyright please inform me at anesthesiatoday@gmail.com and necessary action will be taken soon as possible.
My blog is also non-commercial.



Monday, March 8, 2010

MUSCLE RELAXANTS IN THE ICU.

Muscle relaxants are used in icu to facilitate mechanical ventilation of  the critically ill patients.The drugs commonly used  are pancuronium, vecuronium, atra curium, cisatra curium, and rocuronium.  Muscle relaxants are essential in the management of tetanus, status epilepticus, to provide hyper ventilation in head injury, or after  precise surgical intervention like tracheal anastomosis and vascular anastomosis.These agents are also used to reduce oxygen consumption or to reduce work of breathing in COPD and ARDS(where inflation pressures are high) patients.

Apart from the beneficial effects  the complications of these agents are also of concern and are investigated. These can be classified as  complications due to short term use and long term use

Short term use   
  • Side effects atracurium causing histamine release or hyperkalemia due to suxamethonium
  • Inadequate analgesia or sedation as these components are under estimated when relaxants are used
Long term use
  • Immobility : DVT decubitus ulcers, peripheral nerve injuries.
  • Inability to cough:  retained secretions,  atelectasis and infection
  • Persistent paralysis on stoppage of the drugs "Critical Illness Neuropathy and Critical Illness Myopathy", Steroid induced myopathy.
  • CNS effects of drugs eg: laudanosine causing convulsions
The end result of these complications  are failure to wean from mechanical ventilator, other ventilator associated complications,  residual weakness for life, and health care costs.


Weakness following muscle relaxant use  may be due to persistent neuromuscular blockade by  the drug or its metabolite. eg: The metabolite of vecuronium, 3-des acetyl vecuronium has  80% of the vecuronium activity and may persist for days even after stopping the drug. So critical illness neuromuscular disorder or relaxant myopathy should be suspected  in any patient with difficulty in weaning  from mechanical ventilator or with limb weakness on stopping  the relaxants and sedation. Eventhough not specific, the diagnostic tests used to  establish the diagnosis of critical illness myoneuropathy are EMG, nerve conduction studies and muscle biopsy. Thus icu myopathy or the so called critical illness neuropathy and myopathy are  associated with some critical illness like sepsis or MODS and may be precipitated  with prolonged use of relaxants in large doses.

The other risk factors  which can predispose to weakness are female gender renal failure, disuse atrophy and catabolic states. It has been reported that there is a strong association of corticosteroid use and critical illness myopathy. In patients with asthma flaccid paralysis with increased levels of  creatinine kinase (CK)  levels were observed following mechanical ventilation using muscle relaxants. RD MIller et al., suggests  the dose of muscle relaxants or steroids should be kept minimum in asthmatics on ventilator  and relaxants should be stopped if CK concentrations are increased  The two distinct groups of  critical illness NM disorders are dealtwith here  in detail.
A) Critical Illness Myopathy
  • Persistent paralysis after stopping the relaxants
  • Association of corticosteroid use
  • May be potentiated by B2 agonists as in asthma
  • Muscle histological studies may be needed for establishing a diagnosis and the usual findings include fiber atrophy, mitochondrial defects, myopathy and necrosis
  • Associated renal damage due to myoglobinuria
  • May last for months or years and rarely with residual defects
  • Rehabilitation aided by multidisciplinary team work
B) Critical Illness Neuropathy
  • Seen associated with sepsis and MODS
  • Acute idiopathic , axonal degeneration, in patients with flaccid weakness following long term icu admission as demonstrated by neuro physiologocal studies
  • Can be both sensory and motor neuronal paralysis
  • Nerve conduction studies will be normal(unlike demyelinating syndromes) and CSF will be normal unlike GBS.
  • Usually self limited may last for months or years (but prolonged compared to GBS)
  • Pyridoxine 100-150 mg OD may have protective effect but without strong supporting evidence
Critical illness poly neuropathy should be differentiated from other neuro muscular disorders associated with critical illness
                                      MG                   GBS              CRIT PN
Ocular findings                yes                     no                        no
Fluctuating weakness       yes                     no                        no
Bulbar weakness              yes                     yes                       no
DTR                              intact         depressed             depressed
Autonomic instability       no                      yes                        no
Nerve conduction        normal               abnormal              abnormal

Monitoring of NMB:  by the use of a nerve muscle stimulator and assessing the TOF responses The idea is to administer the  minimum amount of muscle relaxant  needed to achieve the desired therapeutic effect.AT least one twitch of TOF with adequate analgesia and sedation feasible.

Other problems of muscle relaxants

Suxamethonium still remains the best agent of choice for emergency intubation in icu in spite of the undesirable side effects. It produces fast and profound paralysis compared to other agents. Critically ill patients who are supplemented with blood or who have acidosis, are prone for hyperkalemia induced by suxamethonium.Miller suggests prior administration of soda bicarbonate with hyperventilation or rocuronium to replace suxamethonium in acidotic hypovolemic patients.

The other concerns for muscle relaxant use are:

  • Seizures from laudanosine a metabolite of atracurium
  • Hypotension bradycardia and exacerbation of asthma folowing atracurium
Recommendations for the use of muscle relaxants in icu
  • AVOID   the use of relaxant by maximum use of sedation and analgesia and also by manipulation of ventilatory parameters and modes.
  • MINIMISE  the use for less than 48 hrs continuously, boluses than infusion as and when necessary and allowing the patient to come out in between
  • ALTERNATE  isoflurane in place of muscle relaxants or minimise the dose of steroids in asthmatics
REf:  Miller's Anaesthesia 6 th edition, Paul Marino(the icu book) 2nd edition, Oxford Handbok of Criti care, 3rd edition

1 comment:

Anonymous said...

Well... that's interessting but actually i have a hard time figuring it... wonder how others think about this..