1. Presenter : Dr. Kumar Neuromuscular weakness related to
critical illness
2. Introduction Neuromuscular weakness is a common occurrence
in patients who are critically ill, developing in 25 percent of
patients who are in the ICU and ventilated for at least seven days.
Weakness is partly a consequence of improved survival in patients
with multiorgan failure and sepsis, but is also a consequence of
treatments administered in the ICU, including i.v glucocorticoids
and paralytic agents. Neuromuscular weakness in the ICU is most
often due to
3. CRITICAL ILLNESS MYOPATHY The most common form of intensive
care unit (ICU)-acquired myopathy is critical illness myopathy
(CIM). This disorder is also known by other names, including acute
quadriplegic myopathy and thick filament myopathy.
4. Epidemiology and risk factors patients with status
asthmaticus or COPD and 7 percent who receive a liver transplant
develop CIM. Patients with other critical illnesses, such as ARDS,
may also be affected. Each of these disorders is typically
associated with intravenous (IV) glucocorticoid therapy. Triggering
factors may include a higher illness severity index, hyperglycemia,
hyperthyroidism ,
5. Clinical features Critical illness myopathy usually begins
several days after IV glucocorticoid treatment is initiated. The
time of onset of the myopathy may not be known in patients who are
comatose or encephalopathic. The most common presenting features of
CIM are 1. Flaccid quadriparesis that may affect proximal more than
distal muscles 2. Failure to wean from mechanical ventilation
6. Laboratory and electrodiagnostic findings in CIM The
increase in serum CK peaked around four days after initial
treatment with glucocorticoids, and lasted for as long as 16 days.
major nerve conduction findings of CIM are normal to low motor
amplitudes with occasional broadening of the compound muscle action
potential . Phrenic motor amplitudes may also be low. Needle
electromyography shows early or normal full recruitment
7. Direct muscle stimulation- muscles exhibit electrical
inexcitability This inexcitability is due to a defect in muscle
membrane depolarization, which may be related to increased
inactivation of sodium channels at the resting potential
8. pathogenesis of CIM The major histopathologic finding in CIM
is relatively selective loss of myosin, which can be identified as
a lack of reactivity to myosin ATPase in non-necrotic fibers.
atrophy of myofibers, type 2 more than type 1
9. Diagnosis of CIM
10. By definition, patients are or were critically ill, and
weakness should have started after onset of critical illness. 1.
For a definite diagnosis of critical illness myopathy , patients
should have all four major features and one or more supportive
features. 2. For probable critical illness myopathy , patients
should have any three major features and one or more supportive
feature. 3. For possible critical illness myopathy , patients
should have either major features 1 and 3, or 2 and 3, and one or
more supportive feature.
11. Treatment and prognosis of CIM Treatment of CIM is directed
toward 1. discontinuation or reduction of glucocorticoids as soon
as possible, 2. aggressive management of medical conditions 3.
avoidance of additional complications such as venous thrombosis and
4. rehabilitation
12. two studies have reported that intensive insulin therapy
(target blood glucose 80 to 110 mg/dL [4.4 to 6.1 mmol/L]) may
lower the incidence of CIM and CIP among critically ill patients
who remain in the intensive care unit for seven or more days.
Critical illness myopathy is usually reversible over weeks to
months , but leads to prolonged ICU stays and increased length of
hospital stay overall
13. CRITICAL ILLNESS POLYNEUROPATHY 1. second neuromuscular
condition that is commonly acquired in the intensive care unit
(ICU) 2. Critical illness polyneuropathy appears to be a common
complication of severe sepsis 3. mechanism of axonal injury in CIP
is unknown 4. speculation focuses on injury to the microcirculation
of distal nerves, causing ischemia and axonal degeneration. 5.
During the early stages of sepsis, electrical inexcitability due to
sodium channel inactivation may be present in
14. Clinical features of CIP Affected patients manifest a
sensorimotor polyneuropathy characterized clinically by 1. Limb
muscle weakness and atrophy 2. Reduced or absent deep tendon
reflexes 3. Loss of peripheral sensation to light touch and pin
prick 4. Relative preservation of cranial nerve function
15. Laboratory and electrodiagnostic findings Nerve conduction
studies in patients with CIP typically reveal low motor and sensory
amplitudes. Needle EMG may show fibrillation potentials in subacute
to chronic patients. The serum CK levels are normal and muscle
biopsy shows findings consistent with neurogenic atrophy
16. Treatment and prognosis of CIP CIP with mild or moderate
nerve injury, recovery of muscle strength generally occurs over
weeks to months Patients with severe CIP may remain quadriplegic.
treatment of CIP is supportive and includes aggressive management
of sepsis and underlying medical conditions, avoidance of
additional complications such as venous thrombosis, and
17. COMBINED CRITICAL ILLNESS MYOPATHY AND POLYNEUROPATHY
Combined CIM and CIP, sometimes called critical illness
polyneuromyopathy, is increasingly recognized as a cause of
neuromuscular weakness in the ICU. Sepsis and the systemic
inflammatory response syndrome may be a common pathologic mechanism
underlying the development of both CIM and CIP. Nerve conduction
studies may be predictive of neuromuscular dysfunction as early as
72 hours after onset of critical illness.
18. PROLONGED NEUROMUSCULAR JUNCTION BLOCKADE A rare disorder
occurring in the ICU is prolonged neuromuscular junction blockade.
This disorder is related to prolonged use (days) of paralytic
agents, often in the setting of renal or hepatic insufficiency,
leading to prolonged circulation of drug metabolites . These
curare-like paralytic agents bind reversibly to ach receptors on
the motor end-plates of nmjs, thereby inhibiting neuromuscular
transmission
19. The commonly used aminosteroid blocking agents, such as
pancuronium and vecuronium , are normally cleared from the
circulation within several hours, primarily by the liver. in
patients with decreased renal function (creatinine clearance