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Received: 2018.06.10
Accepted: 2018.09.07
Published: 2018.10.26
1358 3 2 8
Rhabdomyolysis with Peripheral Neuropathy:
A Case Series and Literature Review
DE 1 Yoo Jin Lee*
DE 1 Sihyung Park*
DE 1 Yang Wook Kim
DE 2 Kang Min Park
DE 1 Il Hwan Kim
DE 1 Jin Han Park
DE 3 Byeong Ju Lee
DE 1 Bong Soo Park
* These authors contributed equally to this work
Corresponding Author: Bong Soo Park, e-mail: parkbong31@naver.com
Conflict of interest: None declared
Case series
Patients: Female, 59 • Male, 52 • Female, 29
Final Diagnosis: Rhabdomyolysis
Symptoms: Limited movement ability
Medication: —
Clinical Procedure: —
Specialty: Neurology
Objective: Unusual clinical course
Background: Rhabdomyolysis is a syndrome characterized by muscle necrosis and secretion of intracellular muscle components
into the blood circulation. Acute compartment syndrome is a potential complication of severe rhabdomyolysis.
Case Reports: We report 3 cases of compartment syndrome-related peripheral neuropathy in alcoholic individuals with rhab
-
domyolysis. All patients were confirmed to have peripheral neuropathy by electrophysiologic studies.
Conclusions: Patients with underlying metabolic abnormalities, such as those related to long-term alcoholism, should be
aware that rhabdomyolysis is likely to cause neurological abnormalities.
MeSH Keywords: Compartment Syndromes • Peripheral Nervous System Diseases • Rhabdomyolysis
Full-text PDF: https://www.amjcaserep.com/abstract/index/idArt/911602
Authors’ Contribution:
Study Design A
Data Collection B
Statistical Analysis C
Data Interpretation D
Manuscript Preparation E
Literature Search F
Funds Collection G
1 Department of Internal Medicine, Haeundae Paik Hospital, Inje University College
of Medicine, Busan, South Korea
2 Department of Neurology, Haeundae Paik Hospital, Inje University College of
Medicine, Busan, South Korea
3 Department of Rehabilitation Medicine, Pusan National University Hospital,
Busan, South Korea
e-ISSN 1941-5923
© Am J Case Rep, 2018; 19: 1272-1278
DOI: 10.12659/AJCR.911602
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Background
Rhabdomyolysis is a syndrome characterized by muscle necrosis
and secretion of intracellular muscle components into the blood
circulation. Additionally, creatinine kinase levels are markedly
increased and myoglobinuria may occur. Acute compartment
syndrome is a potential complication of severe rhabdomyolysis.
Any condition that increases the intra-compartmental pressure,
such as trauma, ischemia-reperfusion injury, coagulopathy, and
prolonged limb compression, creates the risk for compartment
syndrome development. Metabolic changes associated with
long-term excessive alcohol consumption may also increase
the risk of neuropathy in patients with rhabdomyolysis. We
reviewed 3 cases of peripheral neuropathy accompanied by
rhabdomyolysis in alcoholic individuals. We also investigated
the occurrence of rhabdomyolysis caused by alcohol consump-
tion and the increased risk of neuropathy in cases of rhabdo-
myolysis due to alcohol consumption.
Case report
Three patients had rhabdomyolysis, concomitant compartment
syndrome, and peripheral neuropathy that occurred with long-
term alcohol consumption. Objective neurological examina
-
tions such as electromyography (EMG) and nerve conduction
tests (NCT) were performed for these cases.
Case 1
A 59-year-old alcoholic woman was admitted to our institution
because of limited movement ability of her lower limbs. Nine days
before being admitted, she was found asleep while sitting with
her body in a twisted position on an electric pad. She had fallen
asleep while drinking alcohol and denied using any medication.
She had a normal appearance at 8: 00 pm the previous night and
was found the following morning at 7: 00 am; therefore, her ap-
proximate duration of immobilization was 11 hours. She received
normal saline hydration at the local clinic for 9 days; however,
her movement restriction in the lower limbs did not improve.
Therefore, she presented to our hospital. At the time of admission,
her vital signs were as follows; blood pressure 120/80 mmHg,
Figure 1. There was diffuse mild uptake along both gluteal muscles around the pelvic bone.
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Rhabdomyolysis with peripheral neuropathy
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heart rate 74 beats/min, and body temperature 36.6°C. Her labo-
ratory findings indicated a creatinine level of 1.47 mg/dL, lactate
dehydrogenase (LDH) level of 1219 IU/L, creatine phosphokinase
(CPK) level >10 000 U/L, and ethanol level of 0.9 mg/dL. Despite
hydration and bed rest, her lower-limb movement was still re-
stricted. Using a manual muscle test, her hip flexion and exten-
sion and knee flexion and extension had Medical Research Council
(MRC) grade 4 power (active movement against gravity and re-
sistance), bilateral ankle flexion had MRC grade 0 power, right
ankle extension had MRC 0 grade power (complete paralysis),
and left ankle extension had MRC 1 grade power (minimal con-
traction). She had decreased sensations to touch and pain on
the dorsum muscles of both feet. No ankle jerk or pathologic re-
flexes were observed. A whole-body bone scan was performed
after administration of 25 mCi of Tc99m hydroxy diphosphonate
(HDP). There was diffuse mild uptake along both gluteal mus-
cles around the pelvic bone (Figure 1). Electrophysiologic abnor-
malities suggesting bilateral sciatic nerve lesions were observed
with NCT (Table 1A) and EMG (Table 1B). Therefore, she was di-
agnosed with bilateral sciatic neuropathy associated with rhab-
domyolysis and underwent fluid therapy and rehabilitation. After
44 days, she was discharged without any sequelae. Her labo-
ratory findings at discharge were creatinine 0.72 mg/dL, LDH
272 IU/L, and CPK 253 U/L.
Muscle Insertional activity Rest activity
PSW/fibrillation Recruitment Volitional activity
Both VM Normal 0 Normal NMU
Both TA Increased 2+ –No MUAP
Both PL Increased 2+ –No MUAP
Both TP Increased 2+ –No MUAP
Both GMed Normal 0 Normal NMU
Both BFLH Normal 0 Normal NMU
Both BFSH Increased 2+ Normal NMU
Lt. GCM Increased 2+ –No MUAP
Rt. GCM Increased 2+ Decreased Decreased IP
Lumbar PSM Normal 0 – –
Nerve DSL
(m/s)
S amp
(µV)
DML
(ms)
M amp
(mV)
NCV
(m/s)
F-wave latency
(ms)
Lt. median 3.1 19.5 3.9 12.6 54.9 26.1
Lt. ulnar 2.7 9.0 2.5 11.4 54.9 25.7
Lt. peroneal NR NR NR NR –NR
Lt. sural(S)/tibial(M) NR NR NR NR –NR
Rt. peroneal NR NR NR NR –NR
Rt. sural(S)/tibial(M) 3.7 0.7 3.9 5.0 40.8 50.4
Table 1. Electrophysiologic abnormalities were observed in bilateral sciatic nerve lesions.
(A)
(B)
DSL – distal sensory latency; S amp – sensory amplitude; DML – distal motor latency; M amp – motor amplitude; NCV – nerve
conduction velocity; Lt – left; NR – no response; Rt – right.
PSW – positive sharp wave; VM – vastus medialis; NMU – normal motor unit; TA – tibialis anterior; MUAP – motor unit action
potential; PL – peroneus longus; TP – tibialis posterior; GMed – gluteus medius; BFLH – biceps femoris long head; BFSH – biceps
femoris short head; Lt – left; GCM – gastrocnemius; Rt – right; IP – interference pattern; PSM – paraspinal muscle.
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Rhabdomyolysis with peripheral neuropathy
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Case 2
A 52-year-old alcoholic man was admitted to the Emergency
Department of our institution. He drank alcohol and ingested
sleeping pills (lorazepam 3 mg) the night before he presented
to the Emergency Department. On the morning of admission,
he could not move his left arm or both legs. Dents were found
Nerve DSL
(m/s)
S amp
(µV)
DML
(ms)
M amp
(mV)
NCV
(m/s)
F-wave latency
(ms)
Lt. radial 2.8 6.4 NR NR NR –
Lt. median 3.1 14.4 3.2 18.1 53.5 26.9
Lt. ulnar 2.9 24 2.3 13.3 51.6 30.6
Lt. dorsal ulnar NR NR – – – –
Rt. radial 2.7 18.8 – – – –
Rt. median 3.1 19.8 3.4 23.5 55.1 26.6
Rt. ulnar 3.6 36 2.6 13.9 56.2 26.8
Rt. dorsal ulnar 2.4 11.4 – – – –
Lt. peroneal 3.8 1.2 NR NR NR NR
Lt. sural/tibial 3.6 4.1 3.3 24.1 41.7 48.1
Rt. peroneal 3.9 6.8 3.0 5.4 42.3 47.1
Rt. sural/tibial 3.4 7.4 3.7 18.8 40.6 50.4
Table 2. Electrophysiologic abnormalities were observed in lt. Dorsal ulnar cutaneous nerve, lt. Radial nerve, lt. Superficial and deep
peroneal nerve lesions.
(A)
DSL – distal sensory latency; S amp – sensory amplitude; DML – distal motor latency; M amp – motor amplitude; NCV – nerve
conduction velocity; Lt – left; NR – no response; Rt – right.
Muscle Insertional activity Rest activity
PSW/fibrillation Recruitment Volitional activity
Lt. brachioradialis Increased 2+ –No MUAP
Lt. EDC Increased 2+ –No MUAP
Lt. APB Normal 0 Normal NMU
Lt. FDI Increased 1+ Normal NMU
Lt. TA Decreased 0 – No MUAP
Lt. PL Decreased 0 – No MUAP
Lt. BF, short head Normal 0 Normal NMU
(B)
PSW – positive sharp wave; MUAP – motor unit potential; EDC – extensor digitorum communis; APB – abductor pollicis brevis;
NMU – normal motor unit; FDI – first dorsal interosseous; TA – tibialis anterior; PL – peroneus longus; BF – biceps femoris.
in his left thigh, chest, and face. He had reduced sensation of
the left ulnar distribution, which was accompanied by a tin-
gling sensation. He could not move his left wrist extensor and
finger extensor smoothly and could not lift his left thumb.
Furthermore, he could not move his left ankle dorsiflexor
smoothly. At the time of admission, his vital signs were as fol-
lows: blood pressure 130/75 mmHg, heart rate 68 beats/min,
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Rhabdomyolysis with peripheral neuropathy
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and body temperature 36.8°C. Initial laboratory findings showed
a creatinine level of 1.62 mg/dL, LDH level of 4030 IU/L, CPK
level >10,000 U/L, and ethanol level of 1.1 mg/dL. During NCS
(Table 2A) and EMG (Table 2B), electrophysiologic abnormal-
ities were observed in the left dorsal ulnar cutaneous nerve,
left radial nerve, and left superficial and deep peroneal nerves.
He was diagnosed with complete injury of the left ulnar, radial,
and common peroneal nerves associated with rhabdomyolysis
and underwent fluid therapy and rehabilitation. He was dis-
charged without any sequelae after 14 days. Laboratory find-
ings at discharge were creatinine, 0.79 mg/dL, LDH 383 IU/L,
and CPK 629 U/L.
Case 3
A 29-year-old alcoholic woman was admitted to the Emergency
Department of our institution. She drank alcohol and ingested
sleeping pills (zolpidem 20 mg) the night before admission.
She reported dysesthesia of the right shoulder girdle area
and posterior neck area. During the manual muscle test, right
elbow flexion had MRC grade 4 power (active movement
against gravity and resistance), right elbow extension had MRC
grade 3 power (weak contraction against gravity), right wrist
extension had MRC grade 0 power (complete paralysis), and
right finger extension had MRC grade 1 power (minimal con-
traction). At the time of admission, her vital signs were blood
pressure 110/70 mmHg, heart rate 72 beats/min, and body
temperature 36.7°C. Initial laboratory findings showed a cre-
atinine level of 4.96 mg/dL, LDH level of 1229 IU/L, CPK level
>10 000 U/L, and ethanol level of 1.0 mg/dL. A whole-body
bone scan was performed after administration of 25 mCi of
Tc99m HDP. The study showed diffusely increased soft-tissue
uptake at the right neck, shoulder, and upper arm, suggesting
muscle injury (Figure 2). During NCS (Table 3A) and EMG
(Table 3B), electrophysiologic abnormalities were observed in
the right proximal radial nerve. She was diagnosed with in-
complete axonal injury of the right proximal radial nerve as-
sociated with rhabdomyolysis and underwent fluid therapy
and rehabilitation. After 37 days, she was discharged without
any sequelae. Laboratory findings at discharge were creatinine
0.8 mg/dL, LDH 305 IU/L, and CPK 46 U/L.
Figure 2. There was diffusely increased soft-tissue uptake at the right neck, shoulder, and upper arm, suggesting muscle injury.
1276
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Rhabdomyolysis with peripheral neuropathy
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Discussion
Rhabdomyolysis is a syndrome characterized by muscle ne-
crosis and secretion of intracellular muscle components such
as electrolytes, myoglobin, and creatinine kinase in the blood
circulation. The most common clinical symptoms associated
with rhabdomyolysis are trauma, immobilization, and over-
exertion. Its causes include cardiac surgery, prescription drug
use (such as lipid-lowering drugs), alcohol use, and illegal drug
use (such as cocaine use). Clinical manifestations of rhabdo-
myolysis may include muscle pain, decreased muscle strength,
black urine, and acute renal failure. Acute compartment syn-
drome is a potential complication of severe rhabdomyolysis;
however, compartment syndrome is not a rare finding in rhab-
domyolysis [1,2]. Acute compartment syndrome can occur in
any distinct anatomic compartment bound by unyielding fas-
cial membranes.
Nerve DSL
(m/s)
S amp
(µV)
DML
(ms)
M amp
(mV)
NCV
(m/s)
F-wave latency
(ms)
Lt. radial 2.6 29.1 1.95 4.6 58.8 –
Lt. median 2.5 31.0 2.9 8.5 62.5 23.5
Lt. ulnar 2.3 18.0 2.1 12.3 62.5 23.8
Rt. radial 3.0 3.4 2.5 1.1 54.4 –
Rt. median 2.7 19.4 2.4 9.5 57.7 24.6
Rt. ulnar 2.5 15.6 2.2 13.1 62.2 25.3
Muscle Insertional activity Rest activity
PSW/fibrillation Recruitment Volitional activity
Rt. deltoid Normal 0 Normal NMU
Rt. biceps brachii Normal 0 Normal NMU
Rt. brachioradialis Increased 1+ –No MUAP
Rt. triceps Increased 1+ –No MUAP
Rt. EDC Increased 2+ –No MUAP
Rt. ECR Increased 1+ –No MUAP
Rt. FDI Normal 0 Normal NMU
(B)
PSW – positive sharp wave; Rt – right; NMU – normal motor unit; MUAP – motor unit potential; EDC – extensor digitorum communis;
ECR – extensor carpi radialis; FDI – first dorsal interosseous.
Table 3. Electrophysiologic abnormalities were observed in right proximal radial nerve lesions.
(A)
DSL – distal sensory latency; S amp – sensory amplitude; DML – distal motor latency; M amp – motor amplitude; NCV – nerve
conduction velocity; Lt – left; Rt , right.
The severity of rhabdomyolysis varies. This variability is not
fully understood, but it can be related to physical fitness, mor-
phological characteristics, and sex [3]. Risk factors for acute
compartment syndrome include young age and male sex [4,5].
After achieving complete body growth, the size of the com-
partment is usually fixed; however, young people can have
relatively large volumes of muscles. In contrast, elderly indi-
viduals may have smaller hypotrophic muscles, and their rel-
atively higher blood pressure can provide tolerance to high
tissue pressure [6].
Metabolic changes associated with long-term alcohol con
-
sumption may also increase the risk of neuropathy in patients
with rhabdomyolysis. Alcohol-related rhabdomyolysis has been
attributed to direct toxic effects on muscles and secondary
metabolic changes associated with alcohol abuse. Repeated
administration of ethanol can increase serum CPK activity and
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Rhabdomyolysis with peripheral neuropathy
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produce ultrastructural changes in human skeletal muscles [7].
Furthermore, repeated administration of an alcohol-based diet
to dogs resulted in subclinical myopathy, and ethanol con-
sumption can result in hyperpolarization of the resting trans-
membrane potential of skeletal muscle fibers and a significant
increase in Na-K-ATPase activity accompanied by increased
sodium transport-dependent respiration [8]. With traumatic
rhabdomyolysis, pressure causes necrosis of the muscles, and
diffusion of calcium, sodium, and water into damaged cells
occurs. Combined alcohol-induced direct neurologic abnor-
malities and crush injuries may also increase the risk of neu-
ropathy in patients with rhabdomyolysis.
References:
1. Vanholder R, Sever MS, Erek E, Lameire N: Rhabdomyolysis. J Am Soc Nephrol,
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2. Larbi EB: Drug-induced rhabdomyolysis. Ann Saud Med, 1998; 18: 525–30
3. Kim J, Lee J, Kim S et al: Exercise-induced rhabdomyolysis mechanisms and
prevention: A literature review. J Sport Health Sci, 2016; 324–33
4. McQueen MM, Gaston P, Court-Brown CM: Acute compartment syndrome.
Who is at risk? J Bone Joint Surg Br, 2000; 82: 200–3
Conclusions
We examined 3 cases of peripheral neuropathy in patients
with rhabdomyolysis due to immobilization. Patients with un-
derlying metabolic abnormalities caused by conditions such
as long-term alcohol consumption should be aware that rhab
-
domyolysis is likely to cause neurological abnormalities. More
careful observation is needed for these cases.
Conflicts of interest
None.
5. Clarkson PM, Hubal MJ: Are women less susceptible to exercise-induced
muscle damage? Curr Opin Clin Nutr Metab Care, 2001; 4: 527–31
6. Gelberman RH, Szabo RM, Williamson RV et al: Tissue pressure threshold
for peripheral nerve viability. Clin Orthop Relat Res, 1983; 178: 285–91
7. Perron AD, Brady WJ, Keats TE: Orthopedic pitfalls in the ED: Acute com-
partment syndrome. Am J Emerg Med, 2001; 19: 413–16
8. Ferguson ER, Blachley JD, Carter NW, Knochel JP: Derangements of muscle
composition, ion transport, and oxygen consumption in chronically alco-
holic dogs. Am J Physiol, 1984; 246: 700–9
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Rhabdomyolysis with peripheral neuropathy
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