Blood Supply Classification and Varied Clinical

Transcription

RESEARCH
Blood Supply Classification and Varied Clinical Manifestations of
Skeletal Muscle Infarction
Ya-Wei Lai, MD, Su-Shin Lee, MD, Kao-Ping Chang, MD, PhD, Shu-Hung Huang, MD, Yu-Nan Lin, MD,
Sin-Daw Lin, MD, and Chung-Sheng Lai, MD, PhD
Background: Muscle infarction is a rare complication of spontaneous ischemic
necrosis occurring in skeletal muscle. It is particularly common in patients with
diabetes who have impaired sugar regulation. However, muscle infarction is frequently misdiagnosed due to varied clinical manifestations.
Methods: We presented 3 cases of muscle infarction reported during April 2009
to April 2014. After a comprehensive literature review, we selected 147 muscle
infarction cases from the literature, first investigating the relationships between
type of muscle blood supply and infarcted muscle.
Results: The result indicated that muscle infarction 25.85 % belonged to type I
vascular supply and 61.21% belonged to type II vascular supply, according to
the definition by Mathes and Nahai.
Conclusions: Poor glucose regulation, intense exercise without adequate hydration, vascular disease, and type I and II muscular blood supply were critical predisposing factors. For preventing muscle infarction, we recommend strict glucose
regulation and a gradual increase in exercise with adequate hydration.
patients' demographics including age, sex, underlying disease, clinical
manifestation, biochemistry data, activities before infarction occurrence,
and initial diagnosis.
According to the patterns of blood supply in muscles, Mathes
and Nahai5 classified 5 types of vascular supply: type I, single vascular pedicle; type II, dominant vascular pedicle and minor pedicles; type
III, dominant pedicles; type IV, segmental pedicles; and type V, dominant pedicle with secondary segmental pedicles.
We collected information on DMI cases in which definite muscle
infarction location was indicated based on PubMed beginning in 1999.
The infarcted muscles and the types of muscle blood supply were investigated. Statistical analysis was used to determine the possible relationships between blood supply type and muscle infarction.
RESULTS
Key Words: skeletal muscle infarction, diabetes, vascular classification
(Ann Plast Surg 2015;00: 00–00)
L
imb infarction induced by spontaneous skeletal muscle infarction
is rare. Skeletal muscle, an organ that receives an abundant blood
supply, is at less risk of infarction. However, spontaneous infarction
of skeletal muscles, which is unrelated to atheroembolism or major arterial occlusion in patients with diabetes mellitus, is known as diabetic
muscle infarction (DMI).1,2 Angervall and Stener first described this
tumoriform clinical picture in 1965. Diabetic muscle infarction is rare
and frequently associated with poor disease prognosis and high mortality,3 and the clinical presentation of acute pain, swelling, and a possible
palpable mass may cause physicians to misdiagnose the disorder.4
In this paper, we discuss the clinical images, underlying diseases,
aggravating factors, treatment, and outcomes of 3 muscle infarction
cases. We selected DMI cases from relevant literature and first applied
the vascular classification proposed by Mathes and Nahai5 to analyze
the type of infarcted muscle blood supply. In addition, we determined
the correlations between athletic activities and muscle infarction. The
findings suggest that increased clinical awareness is vital for early diagnosis and appropriate management.
Our study consists of three patients (2 female and 1 male), with
one diagnosed as diabetes mellitus (DM) and one diagnosed as prediabetes. The male patient was healthy and reported no history of systemic
disease. His triceps infarction may have been induced by a congenital
vascular anomaly and enhanced by dehydration and intense muscle action. Of the patients with DM, one had Buerger disease, which aggravated the DMI episode. All of the patients had exercised before the
muscle infarction occurrence, and inadequate fluid supply was noted
in all patients. Tables 1 and 2 list the patients' demographics and possible predisposing factors.
Of the 147 infarcted muscles examined, musculus vastus medialis
[27 (18.37%)] and musculus vastus lateralis [27 (18.37%)] were the most
commonly infarcted muscles. Statistics suggested that 25.85% of the infarcted muscles had type I vascular supply and 61.21% had type II vascular supply (Table 3).
Case Presentation
Case 1
A 46-year-old woman, who had a diagnosis of diabetes for
7 years, had no history of diabetes medication use and had engaged
MATERIALS AND METHODS
We used 3 cases of muscle infarction reported during April 2009
to April 2014 at Kaohsiung Medical University Hospital, investigating
Received September 11, 2014, and accepted for publication, after revision, December
17, 2014.
From the Division of Plastic Surgery, Department of Surgery, Kaohsiung Medical
University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Conflicts of interest and sources of funding: none declared.
Reprints: Chung-Sheng Lai, MD, PhD, Division of Plastic Surgery, Department of
Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University,
19th Floor, 100 Tz-You 1st Rd, Kaohsiung 807, Taiwan. E-mail: [email protected].
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
ISSN: 0148-7043/15/0000–0000
DOI: 10.1097/SAP.0000000000000461
Annals of Plastic Surgery • Volume 00, Number 00, Month 2015
TABLE 1. Patients' Demographics
Case
No.
Buerger
Age/Sex DM Disease
1
2
46/F
80/F
+
+
−
+
3
33/M
−
−
Involved
Muscle
Activity
Before
Attack
Initial
Diagnosis
Gastrocnemius Biking
Hematoma
Gastrocnemius Mountain
DVT
climbing
Triceps
Heavy stuff Tendon
lifting
rupture
F, female; M, male; DVT, deep vein thrombosis.
www.annalsplasticsurgery.com
Copyright © 2015 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
1
Lai et al
TABLE 2. Patients' Laboratory Data
Case No.
HbA1C (%)
TG (mg/dL)
CPK (IU/L)
14.4
6.3
Normal
724
212
Normal
Normal
Normal
1428
1
2
3
after 6 months revealed that the focal lesion in the gastrocnemius muscle had improved, and a slightly heterogeneous lesion with decreased
T2 remained. It indicated both fibrosis and degeneration. However,
poor sugar control was noted at follow-up because the patient complied
poorly. Nine months after the first incident, the patient experienced another incident with similar location and symptoms. The second DMI incident was diagnosed using another MRI examination. The patient was
repeatedly educated on the importance of blood glucose regulation.
HbA1C, glycated hemoglobin.
Case 2
in no routine exercise. She experienced severe pain in her right calf after
cycling for 2.5 hours. According to her memory, she did not take fluid
supplements during the period of exercise. She sought outpatient care
for a rigid mass that had formed in her right calf 2 weeks after the
episode. The patient denied any history of fever, trauma, animal bite,
or infection. An 8 6-cm rigid mass without local heat or reddish skin
was observed (Fig. 1). Initial laboratory workup revealed blood glucose
in which fasting blood sugar was 434 mg/dL and glycated hemoglobin
was 14.4%. In addition, her triglyceride was 724 mg/dL and her cholesterol was 239 mg/dL. Because the physicians assumed she had hematoma, they arranged magnetic resonance imaging (MRI). A T2-weighted
image revealed a high signal lesion over the gastrocnemius muscle of
the right calf and a slightly increased formation of focal collateral circulation in the lateral sural artery (Figs. 2, 3). Diabetic muscle infarction
was diagnosed by the radiologist. Bed rest, analgesic drugs, muscle
relaxants, hydration, and hypoglycemic agents were prescribed. The
symptoms were relieved gradually after 2 months. A follow-up MRI
An 80-year-old woman with Buerger disease and hypertension
experienced acute onset of painful swelling in the left leg after her daily
mountain hike. She was hospitalized because of swelling and pain 5 days
after the incident. Because physicians assumed she had deep vein thrombosis, they performed a series of examinations. Although the data were
within the reference range, triacylglycerol and glycated hemoglobin were
elevated. During her admission, a painful palpable mass was observed.
Magnetic resonance imaging revealed a high signal lesion on
the gastrocnemius muscle in the T2-weighted image. Diabetic muscle
infarction was diagnosed in the patient, and he was prescribed a conservative treatment and intensive glucose control. Symptoms improved
gradually without the assistance of any invasive procedure.
Case 3
A 33-year-old man experienced painful swelling in his left upper
arm after lifting a heavy object (approximately 20 kg) one day at noon.
Because of the extreme temperature that day, he perspired excessively.
TABLE 3. Vascular Type of Infarcted Muscles
Classification
Jelinek et al6 1999
Huang 20107
Litvinov et al19 2012
Arroyave et al18 2013
Lai 20148
Total N (%)
VM
II
26
0
0
1
0
VL
I
26
0
0
1
0
VI
II
20
0
0
0
0
RF
II
14
0
0
0
0
Gastrocnemius
I
7
1
1
0
2
BF
II
10
0
0
0
0
Sartorius
IV
10
0
0
0
0
Adductor
Not classified
9
0
0
0
0
Soleus
II
6
1
0
0
0
Gracilis
II
6
0
0
0
0
Peroneus
II
5
0
0
0
0
Triceps
II
0
0
0
0
1
27
18.37
27
18.37
20
13.6
14
9.52
11
7.48
10
6.80
10
6.80
9
6.12
7
4.76
6
4.08
5
3.40
1
0.68
Muscle Involvement
Total: 147; type I, 25.85%; type II, 61.21%; type III, 0; type IV, 6.8%.
Classification by Mathes and Nahai.5
VI, vastus intermedius; VM, vastus medialis; VL, vastus lateralis; RF, rectus femoris; BF, biceps femoris.
2
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Blood Supply and Skeletal Muscle Infarction
FIGURE 1. A rigid mass 8 cm 6 cm was noted over right
calf area.
He visited the outpatient clinic one week after the incident. Physical
examination revealed a painful mass in the left upper arm. Results
from laboratory data were normal except for creatine phosphokinase:
1428 IU/L. The man was hospitalized because physicians assumed he
had a ruptured tendon with hematoma. Angiography showed no evidence of embolism or thrombosis in his left upper extremities. An
MRI revealed mild swelling in the high-signal adjacent soft tissue in
the long head of the left triceps muscle (Fig. 4). Triceps muscle infarction was diagnosed, and he was given prescribed analgesic medication to control the pain and instructed to hydrate adequately and rest.
Because symptoms improved, the patient was discharged after 10 days.
DISCUSSION
Skeletal muscle infarction in limbs is rare because of abundant
blood supply to the area. Although more than 150 million people have
diabetes worldwide, only a few reports of DMI have been published
since the first incident report in 1965.2–4,6–12 In this paper, we report
FIGURE 2. Upper row, Axial view of MRI with hyperintense
signal. Lower row, Coronal view with infarcted gastrocnemius
and subcutaneous edematous change.
FIGURE 3. Slightly increased formation of focal collateral
circulation of lateral sural artery.
2 cases of DMI in the lower limbs and one case of muscle infarction
in an upper limb. The 3 study patients exercised before the muscle
infarction incident.
The pathogenesis of muscle infarction remains unclear. A previous study suggested that microangiopathy and endothelium-mediated
vasodilation impairment caused by diabetes and vascular disease cause
ischemic change in focal muscles.9 Another researcher posited that a
hypercoagulable state decelerates the blood flow, disrupting the blood
supply to the muscle.9,13 In our first 2 DMI cases, the first patient had
a 7-year history of DM and the other had prediabetes without exhibiting
symptoms of vascular damage. Relevant literature indicates that DMI
typically occurs in patients with mean diabetes duration of approximately 15 years.10 Retinopathy, nephropathy, and neuropathy occurred
in 60%, 80%, and 64% of the patients with DMI, respectively.10 However, a short history of diabetes without tripathy in the patients we reviewed implied poor glucose control; dehydration and other vasculitis
diseases, such as Buerger disease, were critical predisposing factors.
Kingwell et al13 indicated that people with diabetes experience impaired blood flow responses in the legs when exercising because of impaired endothelium-dependent vasodilation. Poor glycemic control and
a poor lipid profile contribute to a limited tolerance to physical exertion
because the working muscles have desaturated.14 Womack et al15 described impaired capillary recruitment by muscles in diabetic patients
during exercise. Intense physical exertion in diabetic patients may be
among the critical factors triggering DMI.
FIGURE 4. Homogeneous hyperintensity was noted over triceps
in T2-weighted image.
3
Lai et al
muscle infarction yet recorded. Poor glucose regulation, intense exercise
without adequate hydration, vascular disease, and types I and II muscular
blood supply were critical predisposing factors. To prevent muscle infarction, we recommend strict glucose regulation and a gradual increase
in exercise with adequate hydration.
ACKNOWLEDGMENT
The authors thank Austin Chen and Wang Hui-Min David for assistance of writing skill in English.
REFERENCES
FIGURE 5. Muscle vascular supply classification by Mathes
and Nahai.5
In addition, blood viscosity plays a role in the possible mechanism of muscle infarction. El-Sayed16,17 and El-Sayed et al16,17 observed that exercise-induced hemoconcentration resulted from fluid
transfer from the blood to interstitial spaces. The acute increase in
whole blood viscosity may affect the microcirculatory blood flow and
oxygen delivery to the tissues.18 Increased blood viscosity may induce
ischemic heart disease and stroke in patients with DMI.19 The patient
in case 3 lifted heavy objects without adequately supplementing fluid
intake on a summer day during which temperatures reached 35°C. We
assumed that intense exercise induced increased blood viscosity and
a lack of adequate hydration caused the ischemic infarction. Diabetic
muscle infarction rarely occurs in the upper limbs. Case 3 was the seventh reported case of muscle infarction in the upper limb in relevant literature7,9 and first upper limb muscle infarction in nondiabetic patient.
Mathes and Nahai5 classified 5 types of muscular blood supply.
Type I muscles are supplied only by one dominant pedicle, whereas
type II muscles are typically supplied by a dominate pedicle and minor
pedicle(s). We assumed that once the major pedicle is occluded, muscle
infarction is more likely to occur in muscles with this type of blood
supply than in muscles of other types. Muscles with types III, IV, and
V blood supply have more vascular pedicles and are therefore at a lower
risk of infarction. We compiled statistics regarding the locations of
muscle infarction, classifying the infarcted muscles according to the
classification by Mathes and Nahai2,6–12 (Fig. 5). Types I and II vascular
anatomies accounted for 87% of the DMI. Except for adductor muscles
that lack obvious classification, the percentage of muscles with types I
and II blood supply can achieve 92.7% (Table 3).
Treatments for muscle infarction in patients with DMI include
nonsteroidal anti-inflammatory drugs, antiplatelet drugs, steroids, surgical intervention, strict blood sugar control, hydration, and sufficient
bed rest. In a recent study, Kapur et al3,10 concluded that there was a
trend favoring medical treatments. Muscle infarction is an uncommon
condition that must be considered when diabetic patients present with
a sudden onset of severe pain and tenderness in muscles with or without a mass. The differential list is extensive and may lead to misdiagnosis. Magnetic resonance imaging examination is noninvasive and
facilitates accurate diagnosis.6,20–22
CONCLUSION
We presented 3 muscle infarction cases. The first patient, diabetic
with poor sugar control, presented with an infarcted gastrocnemius; the
second patient, prediabetic, had Buerger disease and presented with an
infarcted gastrocnemius; and the third patient presented with triceps infarction, which is extremely rare, and was the seventh case of upper-limb
4
1. Pamoukian VN, Rubino F, Iraci JC. Review and case report of idiopathic lower
extremity compartment syndrome and its treatment in diabetic patients. Diabetes
Metab. 2000;26:489–492.
2. Trujillo-Santos AJ. Diabetic muscle infarction: an underdiagnosed complication
of long-standing diabetes. Diabetes Care. 2003;26:211–215.
3. Kapur S, McKendry RJ. Treatment and outcomes of diabetic muscle infarction.
J Clin Rheumatol. 2005;11:8–12.
4. Macgregor JL, Chan P, Schneiderman PI, et al. Diabetic muscle infarction. Arch
Dermatol. 2007;143:1456–1457.
5. Mathes SJ, Nahai F. Classification of the vascular anatomy of muscles: experimental and clinical correlation. Plast Reconstr Surg. 1981;67:177–187.
6. Jelinek JS, Murphey MD, Aboulafia AJ, et al. Muscle infarction in patients with
diabetes mellitus: MR imaging findings. Radiology. 1999;211:241–247.
7. Huang E, Ho CF, Yip PK, et al. Diabetic muscle infarction in a patient with acute
embolic stroke. Neurol Sci. 2010;31:345–347.
8. Lai YW, Lee SS, Chang KP, et al. Blood supply classification and varied clinical
manifestations of skeletal muscle infarction. Ann Plast Surg. 2015. doi: 10.1097/
SAP.0000000000000461.
9. Hachwi RN, Whitaker CH, Felice KJ. Multiple recurrences of diabetic muscle
infarction: case report and literature review. J Clin Neuromuscul Dis. 2003;5:
96–102.
10. Kapur S, Brunet JA, McKendry RJ. Diabetic muscle infarction: case report and
review. J Rheumatol. 2004;31:190–194.
11. Joshi R, Reen B, Sheehan H. Upper extremity diabetic muscle infarction in three
patients with end-stage renal disease: a case series and review. J Clin Rheumatol.
2009;15:81–84.
12. Schattner A, Zornitzki T, Adi M, et al. Painful swelling in the thigh: diabetic muscle infarction. CMAJ. 2009;180:72–74.
13. Kingwell BA, Formosa M, Muhlmann M, et al. Type 2 diabetic individuals have
impaired leg blood flow responses to exercise: role of endothelium-dependent vasodilation. Diabetes Care. 2003;26:899–904.
14. Joshi D, Shiwalkar A, Cross MR, et al. Continuous, non-invasive measurement
of the haemodynamic response to submaximal exercise in patients with diabetes
mellitus: evidence of impaired cardiac reserve and peripheral vascular response.
Heart. 2010;96:36–41.
15. Womack L, Peters D, Barrett EJ, et al. Abnormal skeletal muscle capillary recruitment during exercise in patients with type 2 diabetes mellitus and microvascular
complications. J Am Coll Cardiol. 2009;53:2175–2183.
16. El-Sayed MS. Effects of exercise and training on blood rheology. Sports Med.
1998;26:281–292.
17. El-Sayed MS, Ali N, El-Sayed Ali Z. Haemorheology in exercise and training.
Sports Med. 2005;35:649–670.
18. Brun JF, Varlet-Marie E, Connes P, et al. Hemorheological alterations related to
training and overtraining. Biorheology. 2010;47:95–115.
19. Momtselidze N, Mantskava M, Mchedlishvili G. Hemorheological disorders
during ischemic brain infarcts in patients with and without diabetes mellitus.
Clin Hemorheol Microcirc. 2006;35:261–264.
20. Arroyave JA, Aljure DC, Canas CA, et al. Diabetic muscle infarction: two cases:
one with recurrent and bilateral lesions and one with usual unilateral involvement.
J Clin Rheumatol. 2013;19:126–128.
21. Litvinov IV, Radu A, Garfield N. Diabetic muscle infarction in a 57-year-old male:
a case report. BMC Res Notes. 2012;5:701.
22. Madhan KK, Symmans P, Te Strake L, et al. Diabetic muscle infarction in patients
on dialysis. Am J Kidney Dis. 2000;35:1212–1216.

Blood Supply Classification and Varied Clinical

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