1963 Dittrich – Lumbodorsal fascia and disability

In this article, published in the journal The Lancet, Raymond Dittrich hypothesizes that certain lesions in the lumbodorsal fascia are related to subfascial fat fibrosis and, subsequently, low back pain. HE EMPHASIZES THE ROLE OF FIBRO-FATTY TISSUE in some obscure pains. Despite the author knows and mentions Copeman’s work, he does not agree completely with Copeman’s theories. He even mentions the edematous fat lobules (also named back mice) that they found while performing the surgical technique, but he mentions they do not remove them. They just remove the subfascial fat fibrosis, which he thinks is due to previous traumatic lesions of the fascia.

Dittrich states that the basic anatomical lesion is “a rupture of the lumbodorsal fascia with subfascial fat fibrosis”. This lesion can cause referred pain and referred tenderness; somatic and autonomic nerve symptoms.

He presents 3 distinct clinical syndromes related to SCLEROTOMAS:

-Second lumbar

-First sacral

-6-7-8 Cervical nerves

Diagnosis is verified by local anesthetization of the suspected trigger points.

Treatment consists in surgical correction of the anatomic lesion, with results being satisfactory. They operate 200 patients. It is worthy to mention that, if they found edematous fat lobules (back mice) especially at the edge of the sacrospinalis muscle, they just left them. They just dissected out the fibrofatty tissue between the two layers of the lumbodorsal fascia.

Raymond J. Dittrich published many articles related to this subject previously to this article:

-1952, The Lumbodorsal fascia and chronic backache

-1953, Low back pain-referred pain from deep somatic structure of the back

-1953, Trigger points (editorial) in The Lancet

-1954, Somatic pain and autonomic concomitants reflex sympathetic dystrophy

-1955, Local anesthesia in diagnosis and treatment of low back pain

-1955, Disability of the knee due to referred pain and related phenomena

-1955, The latissimus dorsi syndrome

-1956, Soft tissue lesions as cause of low back pain

-1957, The role of soft tissue lesions in low back pain

-1950, Subfascial fat abnormalities and low back pain

He does NOT mention the peripheral nerves (like the cluneal nerve involvement) despite insisting a lot on the sclerotomal pattern of referred pain.

Lumbodorsal Fascia and Related Structures as Factors in Disability

Raymond J. Dittrich, M.D.

He is a staff physician at the Cambridge State School and Hospital.

Cambridge, Minnesota

October 1963

 

The author has made a study of the pathological condition of the soft tissues in the lower back for a period of years.

The importance of fatty tissue as a factor in pain was emphasized by Copeman and Ackerman, who related the pain to the herniation or edema of fat lobules.

He referred to the “basic fat pattern” of Copeman and Ackerman, Dittrich mentions that the “pattern” had been a useful guide, and said that the most common site of complaint was related to the lateral edge of the erector spinae at the level of the upper margin of the iliac crest, and next to the third sacral vertebra.

The anatomical abnormalities they found were changes in the fascia (defects or thinning, adhesions between fascia and subfascial fat, showing variable degree of fibrosis).

Dittrich hypothesizes that the fascial lesions may be related to muscle contraction. In the lumbar region a portion of the LATISSIUMUS DORSI arises from the fascia; in the sacral region a portion of the GLUTEUS MAXIMUS muscle arises from the fascia. The actions of the muscles can CAUSE TEARS OF THE FASCIA. Maybe the repairing process does not repair completely.

The lesions can produce somatic or autonomic reactions.

 The outstanding feature of the condition is the RUPTURE OF THE LUMBODORSAL FASCIA, with injury and subsequent fibrosis of fat tissue underneath the fascia “rupture of the lumbodorsal fascia with subfascial fat fibrosis”.

 It may remain asymptomatic for an indefinite period of time. And it can give symptoms with certain conditions.

 Dittrich comments on other authors’ work. The background

 -Copeman and Ackerman emphasize the importance of fatty tissue by clinical observation and anatomical dissections. They were convinced that oedema or herniation of fatty lobules could cause pain. He mentions that “Copeman’s basic fat pad pattern” was useful, but it becomes evident that certain parts lack regularity. Dittrich found the anatomic appearance of fat lobules normal except for edema.

 -Dittrich mentions the reference of his work (1950) as an example of some unpredictable and erratic results.

 According to the author, the most common sites of tenderness were 2 sites: over the LATERAL portion of the sacrospinalis muscle at the level of the upper margin of the iliac crest, or at the level of the 3rd lumbar vertebra.

 Around the 3rd sacral vertebra they had a FORTUNATE DISCOVERY of a recent tear of the fascia with shreds of the fascia and bloody fluid appearing in operative wound; the subfascial fat showed normal appearance.

They found the following anatomic abnormalities: changes in fascia consisting in complete defects, marked thinning, adhesions between fascia and fat, and variable degree of fibrosis.

 They hypothesize that the muscle contraction of the latissimus dorsi or the gluteus maximus can cause the development of such lesions by causing tears of the fascia.

 The fascia undergoes then an incomplete process of repair.

 Dittrich suggested that previous studies didn’t have the “complete picture”.

 That’s why they did search in cadavers.

 The pain patterns according to Dittrich

The pain can be referred: thanks to previous studies Kellgren, Lewis, Inman, Sinclair, Weddel, Feidel.

They state that the pain may be referred in any skeletal structure, which receives its sensory nerve supply from the same spinal nerve that impulses arise.

 Pathophysiologic effects: SOMATIC NERVOUS SYSTEM and AUTONOMIC NERVOUS SYSTEM disorders

-The effects of these lumbodorsal fascia lesions can include somatic and autonomic nervous systems.

The somatic nerves effects: pain and tenderness, referred in a sclerotomic portion. The pain and the tenderness are MORE MARKED at the reference sites that in the trigger points.

The referred phenomena were studies by: Kellgren, Lewis, Inman and Saunders, Sinclair, Weddel and Feindel.

 The referred pain differs from the referred tenderness of the TIME OF ONSET.

-Referred pain may appear almost instantly, referred tenderness may require several hours. After local anesthetic of the trigger point, referred pain disappears instantly and referred pain takes several hours.

 Among autonomic effects the most common are vasomotor disorders: cold hands and feet, pallor and sweating, persisting edema of hands and feet.

 Other: sensory defects of anatomic distribution, muscle weakness (due to autonomic dysfunction by reflex reactions).

Clinical considerations

He presents 3 distinguishable syndromes:

1- The midlumbar (second lumbar nerve) syndrome: over the outer portion of the sacrospinalis muscles, at the level of the upper margin of the iliac crest. Pain is located conspicuously in the lower lumbar, upper sacral and sacro-iliac regions and along the iliac crest. Sometimes pain is referred to the groin.

2-The midsacral (first sacral nerve) syndrome: the trigger point is situated in the paraspinal region in the level of the third sacral vertebra.

Pain in the lower back, the gluteal region and the lateral aspect of the thigh, leg and foot. Tenderness is more located in gluteal muscles.

 3-The latissimus dorsi syndrome/sixth, seventh and eight cervical nerves) syndrome. This muscle originates from the lumbodorsal fascia. As the latissiums dorsi is innervated by the sixth, seventh and eight cervical nerves. Then the expanse of affection includes the entire upper extremity, the pectoral muscles, the scalene, the serratus anterior, portions of scapular region, and the spinal and paraspinal structures of the cervicodorsal region.

The knowledge of this could help to identify conditions that present as obscure pains.

 Syndromes can combine and can be bilateral.

 DIAGNOSIS of the lumbodorsal fascia lesions by examination and local anesthetic injection

 The examination:

It is important to define the site and extension of tenderness by examination. It is important to know about the SCLEROTOMES.

Find sites of hyperalgesia or trigger points that are the primary lesions. Compare with the opposite side of the body.

The intensity of tenderness can be less in the trigger point (site of primary lesion).

 The local anesthetization:

Do local anesthetization with 4 to 5 cc of local anesthetic into the suspected trigger point. Deposit the anesthetic into the subfascial tissues. It is possible to evaluate the integrity of the lumbodorsal fascia by the resistance to the penetrating needle.

 The response of the local anesthetic may be immediate or delayed.

 REFERRED PAIN is eliminated promptly within a few minutes after injection.

REFERRED TENDERNESS requires 2-4 hours for disappearance. This may favor the theories that referred tenderness may be related to the liberation of metabolites.

 Sometimes after injection the pain is referred to the other side by patients, then it must be checked.

He estimates that 25-35 per cent of the backaches are due to this type of lesion.

 He mentions that sometimes the pain is just in extremities and that the mechanism could be by “summation of impulses”.

 The local anesthetization is helpful to differentiate it from the lesions from the intervertebral disc that can present in the same clinical way.

TREATMENT of the lumbodorsal fascia lesions: anesthetic injection and surgery

 -Some patients got pain relief for prolonged periods after just local anesthetic. Then it is no further needed.

 -Surgical technique (Dittrich gives an extended detailed explanation of the surgical technique): under local anesthesia, they do a transverse incision about two inches over the trigger site. Through skin and subcutaneous fat, exposing the lumbodorsal fascia. Then they anesthetize the subfascial tissues. They incised the fascia transversely; the subfascial structures consisting of FAT and FIBROUS TISSUE are dissected from the ventral surface of the fascia. The dissection is carried ventrally to a layer of fascia covering the sacrospinalis muscle.

The subfascial fibroadipose layer is dissected free from the deeper layer of fascia and the resected of area about 2×3 inches in diameter. Bleeding vessels are ligated; a soft rubber drain is inserted into the wound for 4-6 days.

 -In the lumbar region it is common to find EDEMATOUS FAT LOBULES near the lateral border of the sacrospinalis muscle. THESE ARE LEFT INTACT. In the sacral region, similar fat masses are encountered in deeper layers. These may also be left in place.

-No serious hemorrhage develops during operation as a rule. But hematomas may follow the operation; removal is carried out 48 hours after removal. They inject 1% procaine into the mass and then the clot can be removed with applicator or eliminated by pressure.

-Patient is discharged 3-4 days after operation. 4-6 weeks to restore normal function.

Analysis of the surgical results

 They operate 200 patients with satisfactory results. Despite they were unable to do proper statistics, some patients presented recurrences, and some got a good response from local anesthetic.

 Dittrich’s DISCUSSION about the lumbodorsal fascia abnormalities

He makes emphasis that fat tissue can be involved and can give answer to many obscure pains in mankind.

 He explains that subfascial fat fibrosis is developed after injuries in the weak fascial points.

 Since the pain follows a sclerotomal pattern, he used the sclerotomal charts of INMAN and SAUNDERS.

 Referred pain should be differentiated from referred tenderness. Referred pain disappears within minutes after anesthetization of the trigger point, referred tenderness takes hours to subsidence. That’s why he advises to reinject the trigger point about two hours after the original anesthetization.

Published in Augut 2018 By Marta Cañis Parera   ORCID iD icon

DITTRICH RJ. LUMBODORSAL FASCIA AND RELATED STRUCTURES AS FACTORS IN DISABILITY. J Lancet. 1963 Oct;83:393-8. PubMed PMID: 14051896