Severe rhabdomyolysis probably induced by quetiapine overdose

A 23-year-old man was taken to the emergency department for attempted suicide (intake of several tablets of quetiapine). At the emergency room, CPK and creatinine levels were 6152 U/L and 1.5 mg/dl respectively. One day later, the patient began with local pain and swelling, weakness and sensory changes in his right forearm.

Due to clinical worsening, four days later an ultrasound was requested, showing an increase in volume and diffuse alteration of the echogenicity of the right forearm, with loss of its normal fibrillar echostructure (fig.1). Soft tissue collections were not defined. The main venous and arterial flows were preserved (fig.2).

The study was completed the same day with an MRI, which confirmed a diffuse involvement of the forearm muscles. This involvement was globally isointense on T1 with a mild and heterogeneous signal hyperintensity in the posterior compartment muscle groups and hyperintense on fluid-sensitive sequences.

It showed a well-defined proximal margin and two patterns of alteration:

• At the proximal level, there was greater signal heterogeneity in long TR sequences and a peripheral enhancement in the post-contrast study, with a central hypocaptant region (fig.4).

• Distally, the signal was more homogeneous and the enhancement diffuse (fig.3).

The set of findings suggested a pattern of rhabdomyolysis, with the more proximal portion showing a more established myonecrosis (fig.5).

Rhabdomyolysis is the clinical situation in which rapid breakdown of skeletal muscle fibres is produced. As a result, there is a leakage of intracellular contents like electrolytes, myoglobin and other sarcoplasmic proteins into the systemic circulation [1]. It is caused by various factors including traumatic, infectious, immunological, electrolyte abnormalities, metabolic diseases, ischemia and immobilization. Multiple cases of rhabdomyolysis due to psychiatric drugs have also been reported, among them the overdose of quetiapine [2, 3, 4]. The CPK concentration is the best indicator of rhabdomyolysis due to serum levels increase proportionally to muscle damage extension. A concentration higher than 5 times the upper limit is diagnostic [5].

Despite the presence of rhabdomyolysis is clinically evident in most cases, it is not clinically diagnosed in 27% of patients. In these cases, MRI can be useful to evaluate the distribution and extension of the affected muscles, the differentiation from other musculoskeletal diseases and prevent serious complications such as peripheral neuropathy [6].

Two types of MRI findings have been described [7, 8]:

Type 1: It is the representation of oedema of the affected muscles in the initial stage of rhabdomyolysis and is non-specific (myositis).

• Homogeneously isointense to hyperintense on T1-weighted.
• Homogeneously hyperintense on T2-weighted and STIR images
• Homogeneously enhanced on contrast-enhanced MR image.

Type 2:  It represents myonecrosis, and is the most specific of rhabdomyolysis.

• Homogeneously or heterogeneously hyperintense on T1-weighted images
• Heterogeneously hyperintense on T2-weighted images
• Rim enhanced on contrast-enhanced MR images of the affected muscles with “stipple sign”, identified as dot-like or linear streaky enhanced foci within an area of rim enhancement.

In both types, the high signal intensities on T1-weighted images may represent the presence of methemoglobin after intramuscular haemorrhage.

Paramagnetic contrast can be used to assess possible collections, in addition to assessing the viability of the muscle tissue and predicting the degree of muscle destruction. Recently, several studies reported that diffusion-weighted imaging and diffusion tensor imaging can help in the detection of muscle ischemia and differentiation between healthy and injured nerves [9, 10]

The treatments are focused on the aetiology of the rhabdomyolysis and on controlling the possible complications such as myoglobinuric acute renal failure and peripheral neuropathy. Our patient received conservative treatment with intense replacement of volume and control of electrolytes imbalance. On the 10th day of admission, an electromyogram was performed that showed signs of sensory-motor axonal neuropathy of the right median, ulnar and radial nerves. Two weeks after admission, the patient was discharged with minimal residual sensory-motor impairment of the right forearm.

Finally, it is interesting to know that MRI does not play a clear role in patient follow-up (no follow-up imaging test was performed on our patient), except for assessing the degree of muscle atrophy and fat infiltration.