Acute Hand Compartment Syndromes after Closed Crush: A Reappraisal

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Acute Hand Compartment Syndromes after Closed Crush: A Reappraisal Francisco del Piñal, M.D., Dr. Med., Francisco Herrero, M.D., Emilia Jado, M.D., Francisco J. García-Bernal, M.D., Dr. Med., and Luis Cerezal, M.D. Santander, Spain Severe crush to the hand is associated with a poor prognosis. The authors investigated the hypothesis that compartment syndrome complicates such injuries. From 1996 to 2000, the authors retrospectively identified 11 patients who, after sustaining a closed crush injury, de- veloped acute hand compartment syndrome. Diagnosis was made on clinical grounds in two patients (the intra- compartmental pressure was not measured) and after clin- ical examination plus measurement of intracompartmen- tal pressure in nine patients. In all cases, the muscle burst out once the fascia was released from the affected com- partment. Clinical clues to elicit the diagnoses were mas- sive hand swelling and tenseness to palpation. Classic symptoms, such as excruciating pain, were absent or their intensity was attributed to the trauma event (in six pa- tients). Classic signs such as intrinsic muscle minus posi- tion and pain on stretching were absent in six and three patients, respectively. In addition, the latter stretch test could not be properly judged in five more patients be- cause of interference by the associated injuries. None of the patients developed contracture or sequela that could be attributed to compartment syndrome. On the basis of this experience, it was concluded that crush injury does not in itself carry a poor functional prognosis, provided that attention is paid to the often-concomitant compart- ment syndrome. Elevated subfascial pressure may be present despite the absence of classic signs and symptoms. (Plast. Reconstr. Surg. 110: 1232, 2002.) Severe crush to the hand has traditionally been associated with a poor functional out- come. 1–4 It should be noted, however, that fail- ure to release swelling muscles confined in closed osteofascial compartments invariably causes muscle death and, subsequently, con- tracture. 5 Irreversible damage to the muscle enclosed in the osteofascial compartments of the hand causes ischemic retraction of the intrinsic muscles, known as Finochietto’s contracture. 6,7 Zancolli 6,8 identified three types of ischemic contracture involving the hand: generalized, which affects all compartments of the hand; localized, which affects only a group of com- partments, mostly referring to the radial- thenar; and atypical, which affects single or unevenly distributed compartments. The syn- drome is characterized by flexion at the meta- carpophalangeal joint, extension of the proxi- mal and distal interphalangeal joints of the fingers, and retropulsion or adduction-palmar abduction of the thumb (in the palm). 6 –10 In this study, we investigated the hypothesis that acute compartment syndrome surrepti- tiously aggravates crush injuries to the hand. Furthermore, we emphasize the need for the surgeon to actively look for compartment syn- drome and to measure the intracompartmen- tal pressure, because the clinical signs may be scant and nonpathognomonic. PATIENTS AND METHODS Over a 5-year period (January of 1996 to December of 2000), the authors retrospectively identified 11 patients who required urgent sur- gical decompression of the intrinsic muscles (all or some) of the hand after sustaining a closed crush. All patients in the study group were male, 20 to 57 years of age, involved in heavy labor, and covered under workers’ com- pensation. Not included in this study were those patients with open crush injuries whose From Instituto de Cirugía Plástica y de la Mano, Hospital Mutua Montañesa, and Clínica Mompía. Received for publication October 26, 2001; revised January 28, 2002. Presented at the 10th Kleinert Society Clinical Reunion, Louisville, Kentucky, September 30 to October 3, 2001. DOI: 10.1097/01.PRS.0000025183.78057.9B 1232

description

www.drpinal.com Francisco del Piñal, M.D., Dr. Med., Francisco Herrero, M.D., Emilia Jado, M.D.,Francisco J. García-Bernal, M.D., Dr. Med., and Luis Cerezal, M.D.

Transcript of Acute Hand Compartment Syndromes after Closed Crush: A Reappraisal

Page 1: Acute Hand Compartment Syndromes after Closed Crush: A Reappraisal

Acute Hand Compartment Syndromes afterClosed Crush: A ReappraisalFrancisco del Piñal, M.D., Dr. Med., Francisco Herrero, M.D., Emilia Jado, M.D.,Francisco J. García-Bernal, M.D., Dr. Med., and Luis Cerezal, M.D.Santander, Spain

Severe crush to the hand is associated with a poorprognosis. The authors investigated the hypothesis thatcompartment syndrome complicates such injuries. From1996 to 2000, the authors retrospectively identified 11patients who, after sustaining a closed crush injury, de-veloped acute hand compartment syndrome. Diagnosiswas made on clinical grounds in two patients (the intra-compartmental pressure was not measured) and after clin-ical examination plus measurement of intracompartmen-tal pressure in nine patients. In all cases, the muscle burstout once the fascia was released from the affected com-partment. Clinical clues to elicit the diagnoses were mas-sive hand swelling and tenseness to palpation. Classicsymptoms, such as excruciating pain, were absent or theirintensity was attributed to the trauma event (in six pa-tients). Classic signs such as intrinsic muscle minus posi-tion and pain on stretching were absent in six and threepatients, respectively. In addition, the latter stretch testcould not be properly judged in five more patients be-cause of interference by the associated injuries. None ofthe patients developed contracture or sequela that couldbe attributed to compartment syndrome. On the basis ofthis experience, it was concluded that crush injury doesnot in itself carry a poor functional prognosis, providedthat attention is paid to the often-concomitant compart-ment syndrome. Elevated subfascial pressure may bepresent despite the absence of classic signs andsymptoms. (Plast. Reconstr. Surg. 110: 1232, 2002.)

Severe crush to the hand has traditionallybeen associated with a poor functional out-come.1–4 It should be noted, however, that fail-ure to release swelling muscles confined inclosed osteofascial compartments invariablycauses muscle death and, subsequently, con-tracture.5 Irreversible damage to the muscleenclosed in the osteofascial compartments ofthe hand causes ischemic retraction of the

intrinsic muscles, known as Finochietto’scontracture.6,7

Zancolli6,8 identified three types of ischemiccontracture involving the hand: generalized,which affects all compartments of the hand;localized, which affects only a group of com-partments, mostly referring to the radial-thenar; and atypical, which affects single orunevenly distributed compartments. The syn-drome is characterized by flexion at the meta-carpophalangeal joint, extension of the proxi-mal and distal interphalangeal joints of thefingers, and retropulsion or adduction-palmarabduction of the thumb (in the palm).6–10

In this study, we investigated the hypothesisthat acute compartment syndrome surrepti-tiously aggravates crush injuries to the hand.Furthermore, we emphasize the need for thesurgeon to actively look for compartment syn-drome and to measure the intracompartmen-tal pressure, because the clinical signs may bescant and nonpathognomonic.

PATIENTS AND METHODS

Over a 5-year period (January of 1996 toDecember of 2000), the authors retrospectivelyidentified 11 patients who required urgent sur-gical decompression of the intrinsic muscles(all or some) of the hand after sustaining aclosed crush. All patients in the study groupwere male, 20 to 57 years of age, involved inheavy labor, and covered under workers’ com-pensation. Not included in this study werethose patients with open crush injuries whose

From Instituto de Cirugía Plástica y de la Mano, Hospital Mutua Montañesa, and Clínica Mompía. Received for publication October 26, 2001;revised January 28, 2002.

Presented at the 10th Kleinert Society Clinical Reunion, Louisville, Kentucky, September 30 to October 3, 2001.

DOI: 10.1097/01.PRS.0000025183.78057.9B

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compartments were spontaneously released bythe injury and required further release of thesame or neighboring compartments. The pres-ence of ragged skin flaps was not a reason forexclusion provided that the underlying com-partments remained intact.

Patients were recruited from two casualtycenters that, between them, receive approxi-mately 600 hand injuries per year, most work-related. In every case, one (or both) of the twofirst surgeons were involved in the assessmentand grading of the signs and symptoms re-ferred to in Table I. The diagnosis of compart-ment syndrome was suspected on the basis ofmarked swelling, disproportionate pain spon-taneously or elicited during the intrinsic test,11

intrinsic minus stance, hypoesthesias or pares-thesias in some or all fingers, and tenseness onpalpation. In addition, a low-threshold policywas maintained in measuring intracompart-mental pressure in any patient whose hand wasswollen, particularly if the mechanism of injurywas a crush. A hand-held digital transducermonitor designed for this purpose (Striker Sur-gical Co., Kalamazoo, Mich.) was used. Mea-surements were performed as suggested by themanufacturer, and 30 mmHg was selected asthe upper normal limit.12–14

Once the diagnosis was made, either on clin-ical grounds in two patients (the intracompart-mental pressure was not measured), or on clin-ical plus recording intracompartmentalpressure in nine, surgery was performed with-out delay (�6 hours after the traumatic eventin all except for case 11, who underwent sur-gery at 12 hours). Release of the affected com-partments was undertaken by means of onethenar, one hypothenar, and two dorsal inci-sions if all compartments were affected (gen-eralized form) or as required in more localizedforms. Detailed information on the surgicaltechnique can be found in the classic text-books.15,16 The carpal tunnel was released onlyif preoperatively the patient referred paresthe-sias in the median nerve distribution and/orthe tissue pressure in the carpal compartmentwas higher than 30 mmHg. In three patients,release of the volar antebrachial fascia was un-dertaken after opening the carpal tunnel (seeDiscussion section). A final patient, who sus-tained a crush to the hand and forearm, re-quired treatment for an associated acute volarforearm compartment (patient 11).

Closure of the carpal canal was done primar-ily in every case to protect the median nerve,

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and efforts were made to attempt primary skinclosure, or to mobilize local tissues, when nec-essary to protect underlying synthesis material.The rest of the wounds were left open to closesecondarily (at approximately 1 week) or toreceive a skin graft as required.

Associated injuries were common (Table I)and, as stated above, some patients presentedbruised and ragged flaps that at times requiredsecondary skin grafts. Losses of muscle masssecondary to the crush event were seen fre-quently and were debrided.

At the latest follow-up, the patients were eval-uated for intrinsic muscle tightness, includingthe Finochietto-Bunnell test,6,9 and were askedto actively place their fingers in intrinsic plusand minus (hook) to assess the contractionand gliding of the interosseus. The width andsuppleness of the first web was compared withthat of the normal side. The patients werequestioned in relation to pain, paresthesias, ordiminished sensation in the median or ulnarnerve distribution. Range of motion and gripstrength were also studied but were found tobe related to the associated injuries and sowere disregarded. The loss of muscle mass oc-casionally noted at the time of debridementalso complicated the results.

RESULTS

Eleven patients were diagnosed with acutehand compartment syndrome: six had the gen-eralized form; three had the localized form (inevery case affecting the thenar and first webspace muscles, and in two cases also affectingthe second web space muscles); and two hadthe atypical form (case 4, the second and thirdweb spaces muscles; case 11, the lateral thenarand hypothenar muscles). Associated compart-ment syndromes included acute carpal tunnel(seven patients), distal third of the forearm(three patients), and volar forearm (one pa-tient) (Table I).

All patients were evaluated at a minimum of6 months (range, 6 months to 41⁄2 years). At thelatest follow-up, all were able to perform theintrinsic plus and minus actively without diffi-culty except for patients 3 and 4. Patient 3 hadgeneralized adherences of the extensor ten-dons over the proximal phalanx fractures,which limited his ability to perform the intrin-sic minus test. Patient 4 had limited range ofmotion in the index finger after a malunitedproximal phalanx fracture he sustained 2 yearsearlier; he had no additional limitation after

the current injury. The width of the first webwas comparable with that of the normal side inall patients. No sensory loss was reported at thelatest follow-up, and two-point discriminationwas comparable with that of the normal side.Patient 5, however, had hypesthesia in the me-dian territory, which slowly improved to nor-mal over a 3-month period. In this patient,during carpal tunnel release the median nervewas found to be hemorrhagic (possibly becauseof the traumatic event), and epineurotomy andhematoma debridement were performed.

All but two patients returned to their prein-jury heavy-labor jobs. Patient 3, a miner, re-jected a tenolysis of the extensor tendons andretired. Patient 6, a mason, complained of wristpain secondary to concomitant intraarticulardistal radius fracture; this patient is currentlyunemployed and pursuing litigation.

DISCUSSION

Multiple etiologic causes have been impli-cated in Finochietto’s ischemic retraction:crush,6,9 tight hand casts,9 proximal arterial in-juries,9 burns,17 massive extravasation from ar-terial or venous lines,18 and others. From ourinvestigations and clinical experience, we be-lieve that three issues deserve discussion: (1)frequency (or rarity in the setting of crushinjury to the hand), (2) clues for diagnosis, and(3) surgical treatment.

Frequency

Eleven patients had pathologic elevation ofthe intracompartmental pressure or a clinicallyapparent acute hand compartment syndromeduring the study period; in all cases the muscleburst out once the fascia was released. Thisfigure is high if one considers the scant litera-ture on the subject11,18–21 and the low frequencyreported in large trauma centers.22 Unfortu-nately, from our study we cannot infer a riskfactor for a compartment syndrome to developafter severe crush.

Persistent joint contractures and stiffness aresometimes seen after severe crush injury to thehand. In our experience, the frequency of el-evated compartment pressures after crush in-juries raises two questions: (1) Are mild (orsevere) forms of untreated compartment syn-drome involved in the crippling sequelae ofthe crushed hand? (2) Could concomitant pro-phylactic release of the hand compartmentsimprove the end result?

The surgeon should not expect to find the

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classic intrinsic plus stance, as seen after isch-emic contracture secondary to proximal vascu-lar injuries or burns, after a crush injury to thehand. In the latter, the scarring in and aroundthe intrinsic muscles, tendons, and digitaljoints, and the deformities secondary to frac-tures, also play a role in the hand stance.Nemethi2 and Wolfort et al.21 already raised thepoint that ischemic contracture of the intrinsicmuscles could be behind the crippled crushedhand. This hypothesis would explain the ap-parent rarity of the syndrome and the poorprognosis of the crushed hand. Also, it wouldillustrate why, when releasing first web contrac-

ture in patients with a crush injury, the firstdorsal interosseus muscle and adductor are re-placed by scar tissue (Fig. 1, above), whereaswhen the cause of the first web contracture is aburn or late-stage reflex sympathetic dystro-phy, the fascia is tight but normal muscle isunderneath (Fig. 1, below).

Our results support that crush injury doesnot always result in a permanently crippledhand: nine of our patients returned to theirprevious work despite all being covered underworkers’ compensation. Immediate fascioto-mies do play a major role, and this indirectlyanswers the second question above.

FIG. 1. (Above) During the first web contracture release, scar tissue can beseen in this patient, who suffered a crush to his hand 1 year previously. (Below)In another patient with a first web contracture after reflex sympathetic dystrophy,normal muscle is seen when the skin and fascia are excised.

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Clues for Diagnosis

Spinner et al.,11 in their classic 1972 article,comment, “A reliable diagnostic harbinger ofan impeding ischemic contracture of the handis the triad of (1) pain, (2) paralysis, and (3)increasing pain when passively stretching theinvolved intrinsic muscle.”

The presence of severe pain has been en-graved in the surgeon’s mind as a clue to mak-ing the diagnoses of compartment syndromedespite that prominent authors in the field havefound this symptom to be unreliable.13,23–27 In our

series, the pain reported by the patients couldbe easily explained by the traumatic event insix of them. The intrinsic stretch test11,21 was attimes impossible to perform because of theassociated injuries (Table I), and the elicitedpain was difficult to discern from that second-ary to muscular contusion28 in several more ofthe cases. Palsy is agreed to be too late a sign.29

Spinner et al.11 further stated, “The hand isusually grossly edematous. . .in the intrinsic mi-nus posture.” The intrinsic minus stance hasbeen considered diagnostic of acute hand com-

FIG. 2. Poor correlation among hand swelling, intrinsic minus posture, and intracompart-mental pressures can be seen in these examples. (Above, left) Severe swelling, intrinsic minusposture, and intracompartmental pressure of 13 mmHg. (Above, right) Severe swelling, intrinsicplus position, and intracompartmental pressure of 66 mmHg (case 10). (Below) Printer rollerinjury: severe swelling, mild intrinsic minus stance, and intracompartmental pressure of 15mmHg.

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partment syndrome11,18,21,30; however, we havefound this to be not always so (Fig. 2), partic-ularly when only the radial part of the hand isaffected. By the same token, in our series se-vere swelling had a sensitivity of 100 percent,but the specificity was very low; we particularlyemphasize the unspecificity of pitting edema10

compared with tense swelling.18 We not onlyhad patients with massive edema and otherconditions unrelated to crush, but we also hadpatients with crush plus edema and low com-partmental pressure measurements (Fig. 2, be-low). Despite some exceptions,17 tense swellingwas very helpful in reaching and following thediagnoses. Furthermore, and adding moreconfusion, severe swelling may cause an intrin-sic minus stance by itself because of the elastictraction of the skin.31

Whitesides et al.,23 Matsen et al.,32 andMubarak et al.12 presented reliable methods torecord the interstitial tissue pressure for thediagnosis of an impeding compartment syn-drome. However, marked differences exist asto the threshold value for performing a fas-ciotomy, ranging from an absolute 15 mmHg18

to 40 to 50 mmHg (or 20 mmHg below diastol-ic).23 We choose 30 mmHg,12–14 irrespective ofthe blood pressure and age of the patient,because susceptibility of the muscle to addi-tional damage after the crush event may bedecreased.33 Despite interest in recording in-tracompartmental pressure, the surgeonshould not hesitate to open a compartmentthat looks suspicious.22,29 The herniation of themuscle mass during fasciotomy will confirmthe diagnosis.

The clinical part of the study was limited byits dependency on such subjective data as “mas-sive” swelling, “excruciating” pain, tenseness,and so forth. Nevertheless, in every case thepatients were examined and assessed bythe same two surgeons, giving homogeneityto the grading scales referred to in Table I.

Surgical Treatment

Apart from those compartment syndromescaused by massive fluid extravasation in whichnonsurgical treatment (e.g., manual pumping)may have a role,30 once the diagnosis has beenmade, immediate surgical decompression ofthe affected compartments (and subcompart-ments34) should be performed without delay.26

Release of the carpal canal, as recommendedby Ouellette and Kelly,18 was not universallyperformed; rather, it was considered only when

signs and symptoms pointed to acute carpaltunnel syndrome.35–38

In three patients the distal volar forearm wasfound to be tense on palpation. In two pa-tients, measurements taken at the distal andproximal volar forearm levels yielded patho-logic values distally (average, 60) and normalvalues39 proximally (average, 18). All had con-comitant acute carpal tunnel syndrome, andafter opening the carpal canal, further releaseof the distal antebrachial fascia was performedin an attempt to decompress a hypotheticaldistal forearm compartment. Muscle, mainlyflexor carpi ulnaris and adjacent flexor super-ficialis, bulged through the incision, makingprimary closure impossible (Fig. 3). The fasciaof the pronator quadratus40,41 was also released,but the muscle was found to be normal. Reser-vations may arise as to the existence of thecompartment referred to above, because thereis no close space at this level. However, other“open” compartments, such as the carpal tun-nel,35–38 have been described in the literatureand found consistently in experiments.42 Thesyndrome may in fact be a form termed byGardner as “sublimis syndrome.”43 Rather than

FIG. 3. In patient 5, generalized hand compartment plusacute carpal tunnel plus distal forearm compartment (sub-limis compartment). Note the muscles bulging through thethenar and hypothenar incisions and the impossibility ofclosing the distal forearm incision.

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describe a new entity, we hypothesize that byreleasing the distal antebrachial fascia, the sur-geon may abort the vicious cycle of increasedcapillary permeability-edema-ischemia and theprogression to a full-blown volar forearm com-partment syndrome. Recognition of the subli-mis-distal forearm compartment syndrome willexplain the different values recorded in theproximal forearm and distal forearm in twopatients (in the other patient, no measure-ments were taken proximally). It will also ex-plain why some forms of carpal tunnel syn-drome that occur after “simple” Colles fracturedo not respond to conventional release inas-much as the median nerve is actually com-pressed “three inches above the wrist,” as de-scribed by Lewis.44

In summary, any hand crush injury accom-panied by massive swelling and tenseness onpalpation should alert the surgeon to the pos-sibility of acute hand compartment syndrome,despite the absence of classic signs and symp-toms. We recommend that practitioners sys-tematically record intracompartmental pres-sure in any patient with a severe crush injury toall or part of the hand, and that a fasciotomy beroutinely considered, inasmuch as we havefound that the incidence of hand compart-ment syndrome is much higher than might beexpected from the literature. From our inves-tigations we further conclude that if the con-comitant compartment syndrome is appropri-ately treated, crush injury to the hand carries aprognosis as bad as that of the associated inju-ries. We firmly believe that occult-unrecog-nized compartment syndromes are involved inthe frozen hand, first web retraction, limitedmotion, and other sequelae attributed to the“crush hand syndrome.”

Francisco del Piñal, M.D., Dr. Med.Calderón de la Barca 16-entloE-39002 Santander, [email protected]

REFERENCES

1. Mason, M. L., and Bell, J. L. The crushed hand. Clin.Orthop. 13: 84, 1959.

2. Nemethi, C. E. Crushing injury to the hand: Preventionof ischemic contracture. Calif. Med. 90: 207, 1959.

3. Entin, M. A. Crushing and avulsing injuries of the hand.Surg. Clin. North Am. 44: 1009, 1964.

4. Carter, P. R. Crush injury of the upper limb: Early andlate management. Orthop. Clin. North Am. 14: 719,1983.

5. Jepson, P. N. The classic: Ischemic contracture. Exper-imental study. Clin. Orthop. 113: 3, 1975.

6. Zancolli, E. Finochietto’s ischemic contracture and

nonischemic intrinsic-plus deformities. In E. Zancolli(Ed.), Structural and Dynamic Bases of Hand Surgery, 2ndEd. Philadelphia: Lippincott, 1979. Pp. 284–313.

7. Buck-Gramcko, D. La rétraction ischémique de la main.In R. Toubiana (Ed.), Traité de Chirurgie de la Main, Vol.5. Paris: Masson, 1995. Pp. 104–116.

8. Zancolli, E. A. Ischemic contractures. In J. G. McCarthy,J. W. May, and J. W. Littler (Eds.), Plastic Surgery: TheHand, Vol. 8. Philadelphia: Saunders: 1990. Pp. 5033–5052.

9. Bunnell, S., Doherty, E. W., and Curtis, R. M. Ischemiccontracture, local, in the hand. Plast. Reconstr. Surg. 3:424, 1948.

10. Smith, R. J. Intrinsic contracture. In D. P. Green, R. N.Hotchkiss, and W. C. Pederson, (Eds.), Green’s Oper-ative Hand Surgery, Vol. 1, 4th Ed. New York: ChurchillLivingstone 1999. Pp. 604–618.

11. Spinner, M., Aiache, A., Silver, L., and Barsky, A. J. Im-pending ischemic contracture of the hand: Early di-agnosis and management. Plast. Reconstr. Surg. 50: 341,1972.

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