Thread by @ElieNaddaf3

Since #COVID hit, we're hearing a lot about critical illness #myopathy (CIM). Follow this tweetorial that will cover the basic aspect of CIM. Photos below are from a patient with COVID-related CIM.

CIM is a syndrome rather than a distinct entity. It refers to patients who develop a myopathy while being critically ill. The classic characteristic histologic finding is that of "myosinolysis" or loss of myosin.

As the muscle fiber type is determined by the myosin heavy chains, loss of myosin results in "unclassifiable" fibers. Biopsy photos show ATPase reaction at pH9.4 (left), type 2 in dark brown (type 1 light brown), and pH 4.3 (right) with type 1 in dark brown (type 2 pink).

Arrows represent examples of fibers that lost their histochemical fiber type because of myosin loss. They're neither type 1 nor type 2.

Patients can also have a varying degree of necrosis, and subsequently varying CK levels, that may reach 1000s range. This may represent a degree of rhabdomyolysis. CK level is elevated in more than 50% of patients.

The main characteristic finding on electrodiagnostic testing, is prolongation of CMAP duration. Loss of muscle fiber excitability is one hypothesis for underlying pathogenesis. Photo below: Allen et al.2008 @MuscleAndNerve (A:normal CMAP, B: prolonged CMAP with loss of +ve tail)

Risk factors to develop CIM include:
Prolonged ICU stay
Mechanical ventilation
Sepsis
Use of corticosteroids or neuromuscular blockade agents

Which one is the most important diagnostic step when CIM is suspected:
A. EMG
B. CK level
C. Muscle biopsy
D. None of the above
Answer is D: It is "obtaining a detailed history" proving the patient had normal strength prior to admission.

Treatment is supportive and there is NO (NO NO NO) indication for immunotherapy. NO NO NO
@MedTweetorials #MedEd #NeuroTwitter #CriticalCare #Muscle #COVID19 @mayoneurores @MayoFL_NeuroRes @UW_Neurology #Pathology @TheMyositisAssc