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“measuring IAP when any known risk factor for IAH/ACS is present in a critically
ill or injured patient”, and “use of protocolized monitoring and management of IAP
versus not.” Furthermore, they issued a strong negative recommendation: “We could
make no recommendation regarding the prophylactic use of the open abdomen”.
A recent paper compared 79 patients treated with a primarily OA after OSR for
RAAA at a centre performing this as a routine, compared to a propensity scorematched control group of 148 patients treated at other centres in which 73% had the
abdomen was closed at the end of the procedure [28]. There was no difference in
mortality or post-operative complications, thus no benet associated with a routine
practice of leaving all patients open could be demonstrated.
Our policy in Uppsala, Sweden, is to leave the patient open primarily after OSR
of a RAAA only if the abdomen is tense and difcult to close, which occurs in
approximately 5–10% of cases. However, almost all patients with RAAA nowadays
are treated with EVAR.We monitor IAP in the OR (which is of particular importance after EVAR), every hour for 4 h, followed by every 4h for the rst 48 h.
Monitoring is performed more frequently when there is IAH, and DL is performed
on demand. In a review article adapting the WSACS Guidelines to vascular surgery,
this treatment algorithm was described in more detail [25].
M. Björck
19.8 Management ofthePatient withOpen Abdomen (OA)
How to care for the patient who needs a period of OA treatment is a complex issue.
The rst issue is how to manage the open abdomen itself: maintain a sterile environment, keep the intestines moist and protected from injury, protect the abdominal
wall, and enable closure as soon as possible. A classication system of the open
abdomen was developed in 2009, in order to facilitate training and research [29],
and later updated in 2016 [30]. Preventing and controlling contamination, as well as
lateralisation of the abdominal wall, are the key elements to enable closure of the
abdomen as soon as possible [4, 29–31].
The problem of lateralization was dened and highlighted in the Updated
Consensus document [4]: “Lateralization of the abdominal wall is the phenomenon
where the musculature and fascia of the abdominal wall, most exemplied by the
rectus abdominis muscles and their enveloping fascia, move laterally away from the
midline with time.” It is also included in the classication system of OA [29, 30].
The importance of closing the abdomen as soon as possible to maintain a sterile
environment was illustrated by the results from Helsinki, Finland [32]. They used a
temporary abdominal closure (TAC) device including continuous negative pressure
(the VACM method, see below). The OA was progressively colonized and 80% of
the patients had positive bacterial cultures after 2weeks of OA treatment.
The choice of TAC has attracted much attention, and multiple solutions have
been developed, ever since the rst report in the scientic literature of leaving the
abdomen open, in 1897 [33]. An important innovation was developed by paediatric
surgeons, who started to repair omphalocele in the 1940s, using silastic coverage of
19 Abdominal Compartment Syndrome andOpen Abdomen Treatment
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449
the intestines, a rst generation of plastic. A similar system was later popularized in
trauma surgery by the Colombian invention of the Bogotá bag, using the plastic bag
from a drip that is sutured to the skin or the fascia. This system works well for a few
days, but during a more prolonged treatment (which is often necessary after AAA
repair) three major problems develop. Two of those were solved by the later development of the vacuum pack technique, developed in 1995 by Barker et al. in
Philadelphia [34]. The active suction prevented leakage of uids from the OA, and
the surgical towels covered with plastic prevented adhesions forming between the
intestines and the abdominal wall. This system was further rened by a commercially available ready-made system, (V.A.C.® Abdominal Dressing System; KCI,
USA). Later other negative pressure systems were developed by different suppliers.
A third problem, the lateralization of the abdominal wall, remained however,
making it difcult to close patients who had been treated with OA for at least 5days.
This was the reason why a novel method was developed in Uppsala and Malmö,
Sweden; the Vacuum-assisted wound closure and mesh-mediated fascial traction
(VACM) method. The pilot experience of VACM was published in 2007 [35]. This
is a combination of the commercially available VAC system (later replaced by the
ABThera system) with a prolene mesh that is sutured to the fascial edges to permit
an active traction towards the midline (details shown in Fig.19.2). A multicentre
study of this technique (including only patients requiring OA for at least 4days)
showed an 89% primary delayed fascial closure rate after a median time of 15days
Fig. 19.2 A schematic drawing of the VACuum-assisted wound closure and Mesh-mediated fascial traction (VACM) system: (1) The bowel. (2) The plastic sheet covering and protecting the
intestines. (3) The abdominal wall. (4) The rectus abdominis muscle that was divided in the midline at the primary laparotomy. (5) Prolene mesh sutured to the fascial edges, to be advanced
toward the midline and removed progressively. (6) Black foam. (7) The track-pad transmitting the
negative pressure into the system
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M. Björck
with OA [36], and in a sub-group analysis of those treated for aortic disease this
gure was 100% [18]. These results have been repeated independently at other
major centres [37, 38], as well as in a large multicentre study on patients treated for
ACS after AAA repair [39], and is now the preferred TAC method in many centres
world-wide.
19.9 Prognosis
The overall mortality in patients who develop ACS after AAA repair is high. In the
national Swedish study of 6612 patients, the 30day mortality rate after RAAA was
42% among those who developed ACS compared to 24% without ACS.At 1year
mortality was 51% versus 32% [16]. After intact AAA repair, 30day mortality was
12% with ACS versus 1.8% without. At 1year mortality was 28% versus 6%. When
ACS developed, renal failure, multiple organ failure, intestinal ischaemia, and prolonged intensive care stay were all very much more frequent. Interestingly, morbidity and mortality were similar, regardless of the primary surgical technique (OSR or
EVAR), if the patient developed ACS.
Those results are actually rather encouraging, since untreated ACS has a mortality approaching 100%. Perhaps the fact that ACS has been recognized and treated
for many years in Sweden is one of the explanations why survival after RAAA has
increased over time [40].
19.10 Conclusion
In conclusion, IAH and ACS are common and life threatening complications after
aortic surgery. Preventing and treating this complication in a timely way, when it
occurs despite prevention, are important parts of any strategy aiming at improving
outcomes after aortic surgery, whether by an open or endovascular approach.
References
1. Kron IL, Harmon PK, Nolan SP.The measurement of intra-abdominal pressure as a criterion
for abdominal re-exploration. Ann Surg. 1984;199:28–30.
2. Malbrain MLNG, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, de Waele J, etal. Results
from the international conference experts on intra-abdominal hypertension and abdominal
compartment syndrome. I.Denitions. Intensive Care Med. 2006;32:1722–32.
3. Cheatham ML, Malbrain MLNG, Kirkpatrick A, Sugrue M, Parr M, de Waele J, etal. Results
from the international conference experts on intra-abdominal hypertension and abdominal
compartment syndrome. II.Recommendations. Intensive Care Med. 2007;33:951–62.
4. Kirkpatrick A, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Kuelenaer B, etal.
Intra-abdominal hypertension and the abdominal compartment syndrome: updated consen-
19
https://t.me/medicina_free
Abdominal Compartment Syndrome andOpen Abdomen Treatment
sus denitions and clinical practice guidelines from the World Society of the Abdominal
Compartment Syndrome. Intensive Care Med. 2013;39:1190–206.
5. Platell CF, Hall J, Clarke G, Lawrence-Brown M.Intra-abdominal pressure and renal function
after surgery to the abdominal aorta. Aust N Z J Surg. 1990;60:213–6.
6. Djavani K, Wanhainen A, Björck M. Intra-abdominal hypertension and abdominal com-
partment syndrome following surgery for ruptured abdominal aortic aneurysm. Eur J Vasc
Endovasc Surg. 2006;31:581–4.
7. Makar RR, Badger SA, O’Donell ME, Loan W, Lau LL, Soong CV.The effects of abdominal
compartment hypertension after open and endovascular repair of a ruptured abdominal aortic
aneurysm. J Vasc Surg. 2009;49:866–72.
8. Djavani K, Wanhainen A, Valtysson J, Björck M. Colonic ischaemia and intra- abdominal
hypertension following open repair of ruptured abdominal aortic aneurysm. Br J Surg.
2009;96:621–7.
9. Mayer D, Rancic Z, Meier C, Pfammatter T, Veith FJ, Lachat M. Open abdomen treat-
ment following endovascular repair of ruptured abdominal aortic aneurysms. J Vasc Surg.
2009;50:1–7.
10. Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Valdivia A, Sailors RM, et al. Supra-
normal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch
Surg. 2003;138:637–43.
11. Mell MW, O’Neil AS, Callcut RA, Acher CW, Hoch JR, Tefera G, Turnipseed WD.Effect of
early plasma transfusion on mortality in patients with ruptured abdominal aortic aneurysm.
Surgery. 2010;148:955–62.
12. Volodos NL, Shekhanin VE, Karpovich IP, Troian VI, Gur’ev IuA. [A self-xing synthetic
blood vessel endoprosthesis]. Vestn Khir Im I I Grek. 1986;137:123–125.
13. Volodos NL. The 30th anniversary of the rst clinical application of endovascular stent-
grafting. Eur J Vasc Endovasc Surg. 2015;49:495–7.
14. Ohki T, Veith FJ. Endovascular grafts and other image-guided catheter-based adjuncts to
improve the treatment of ruptured aortoiliac aneurysms. Ann Surg. 2000;232:466–79.
15. Beck AW, Sedrakyan A, Mao J, Venermo M, Faizer R, Debus S, etal.; International Consortium
of Vascular Registries. Variations in abdominal aortic aneurysm care: a report from the
International Consortium of Vascular Registries. Circulation. 2016;134:1948–1958.
16. Ersryd S, Djavani-Gidlund K, Wanhainen A, Björck M.Abdominal compartment syndrome
after surgery for abdominal aortic aneurysm: a nationwide population-based study. Eur J Vasc
Endovasc Surg. 2016;52:158–65.
17. Ersryd S, Djavani Gidlund K, Wanhainen A, Smith L, Björck M. Abdominal compartment
syndrome after surgery for abdominal aortic aneurysm: subgroups, risk factors and outcome.
Eur J Vasc Endovasc Surg. 2019;58(5):671–9.
18. Sörelius K, Wanhainen A, Acosta S, Svensson M, Djavani-Gidlund K, Björck M.Open abdo-
men treatment after aortic aneurysm repair with vacuum-assisted wound closure and meshmediated fascial traction. Eur J Vasc Endovasc Surg. 2013;45:588–94.
19. De Waele JJ, Kimball E, Malbrain M, Nesbitt I, Cohen J, Kaloiani V, et al. Decompressive
laparotomy for abdominal compartment syndrome. Br J Surg. 2016;103:709–15.
20. Hörer T, Skoog P, Pirouzram A, Larzon T. Tissue plasminogen activator–assisted hematoma
evacuation to relieve abdominal compartment syndrome after endovascular repair of ruptured
abdominal aortic aneurysm. J Endovasc Ther. 2012;19:144–8.
21. Reintam Blaser A, Starkopf J. Should we use early enteral nutrition in all intensive care
patients? Int J Abdom Res. 2013;1:59–63.
22. Reintam Blaser A, Björck M, De Keulenaer B, Regli A.Abdominal compliance: a bench-to-
bedside review. J Trauma Acute Care Surg. 2015;78:1044–53.
23. Abouassaly CT, Dutton WD, Zaydfudim V, Dossett LA, Nunez TC, Fleming SB, et al.
Postoperative neuromuscular blocker use is associated with higher primary fascial closure
rates after damage control laparotomy. J Trauma. 2010;69:557–61.
24. Papazian L, Forel J-M, Gacouin A, etal. Neuromuscular blockers in early respiratory distress
syndrome. N Engl J Med. 2010;363:1107–16.
451
452
https://t.me/medicina_free
25. Björck M, Wanhainen A.Management of abdominal compartment syndrome and the open
abdomen. Eur J Vasc Endovasc Surg. 2014;47:279–87.
26. IMPROVE Trial Investigators. Comparative clinical effectiveness and cost-effectiveness of
endovascular strategy v open repair for ruptured abdominal aortic aneurysm: three year results
of the IMPROVE randomised trial. BMJ. 2017;359:j4859.
27. Oelschlager BK, Boyle EM, Johansen K, Meissner MH.Delayed abdominal closure in the
management of ruptured abdominal aortic aneurysms. Am J Surg. 1997;172:411–5.
28. Smidfelt K, Nordanstig J, Wingren U, Bergström G, Langenskiöld M.Routine open abdomen
treatment compared with on-demand open abdomen or direct closure following open repair of
ruptured abdominal aortic aneurysms: a propensity score-matched study. SAGE Open Med.
2019;7:2050312119833501.
29. Björck M, Bruhin A, Cheatham M, Hinck D, Kaplan M, Manca G, etal. Classication, an
important step to improve the management of patients with an open abdomen. World J Surg.
2009;33:1154–7.
30. Björck M, Kirkpatrick AW, Cheatham M, Kaplan M, Leppäniemi A, De Waele JJ.Amended
classication of the open abdomen. Scand J Surg. 2016;105:5–10.
31. Björck M, D’Amours SK, Hamilton AER. Closure of the open abdomen. Am Surg.
2011;77:S58–61.
32. Rasilainen SK, Mentula PJ, Leppäniemi AK.Microbial colonization of open abdomen in criti-
cally ill surgical patients. World J Emerg Surg. 2015;10:25.
33. McCosh AJ II.The treatment of general septic peritonitis. Ann Surg. 1897;25:687–97.
34. Brock WB, Barker DE, Burns RP.Temporary closure of open abdominal wounds: the vacuum
pack. Am Surg. 1995;61:30–5.
35. Petersson U, Acosta S, Björck M. Vacuum-assisted wound closure and mesh-mediated
fascial traction—a novel technique for late closure of the open abdomen. World J Surg.
2007;31:2133–7.
36. Acosta S, Bjarnason T, Pettersson U, Pålsson B, Wanhainen A, Svensson M, etal. Multicentre
prospective study of fascial closure rate after open abdomen with vacuum and mesh-mediated
fascial traction. Br J Surg. 2011;98:735–43.
37. Seternes A, Myhre HO, Dahl T.Early results after treatment of open abdomen after aortic
surgery with mesh traction and vacuum-assisted wound closure. Eur J Vasc Endovasc Surg.
2010;40:60–4.
38. Rasilainen SK, Mentula PJ, Leppäniemi AK. Vacuum and mesh-mediated fascial trac-
tion for primary closure of the open abdomen in critically ill surgical patients. Br J Surg.
2012;99:1725–32.
39. Acosta S, Seternes A, Venermo M, Vikatmaa L, Sörelius K, Wanhainen A, etal. Open abdomen
therapy with vacuum and mesh-mediated fascial traction after aortic repair—an international
multi-centre study. Eur J Vasc Endovasc Surg. 2017;54:697–705.
40. Mani K, Björck M, Wanhainen A.Changes in the management of infrarenal abdominal aortic
aneurysm disease in Sweden. Br J Surg. 2013;100:638–44.
M. Björck
Further Reading
Acosta S, Seternes A, Venermo M, Vikatmaa L, Sörelius K, Wanhainen A, Svensson M, Djavani K,
Björck M.Open abdomen therapy with vacuum and mesh-mediated fascial traction after aortic
repair—an international multi-centre study. Eur J Vasc Endovasc Surg. 2017;54:697–705.
Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Valdivia A, Sailors RM, etal. Supra-normal
trauma resuscitation causes more cases of abdominal compartment syndrome. Arch Surg.
2003;138:637–43.
Abdominal Compartment Syndrome andOpen Abdomen Treatment
https://t.me/medicina_free
19
Björck M, Bruhin A, Cheatham M, Hinck D, Kaplan M, Manca G, Wild T, Windsor A.Classication,
an important step to improve the management of patients with an open abdomen. World J Surg.
2009;33:1154–7.
Djavani K, Wanhainen A, Valtysson J, Björck M.Colonic ischaemia and intra-abdominal hyperten-
sion following open repair of ruptured abdominal aortic aneurysm. Br J Surg. 2009;96:621–7.
Ersryd S, Djavani Gidlund K, Wanhainen A, Smith L, Björck M.Abdominal compartment syn-
drome after surgery for abdominal aortic aneurysm: subgroups, risk factors and outcome. Eur
J Vasc Endovasc Surg. 2019;58(5):671–9.
Kirkpatrick A, Roberts DJ, De Waele J, Jaeschke R, Malbrain MLNG, De Kuelenaer B, Duchesne
J, Björck M, etal. Intra-abdominal hypertension and the abdominal compartment syndrome:
updated consensus denitions and clinical practice guidelines from the World Society of the
Abdominal Compartment Syndrome. Intensive Care Med. 2013;39:1190–206.
Mell MW, O’Neil AS, Callcut RA, Acher CW, Hoch JR, Tefera G, Turnipseed WD.Effect of early
plasma transfusion on mortality in patients with ruptured abdominal aortic aneurysm. Surgery.
2010;148:955–62.
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Chapter 20
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Pathophysiology andManagement ofLimb
Compartment Syndromes
DavidLindström andCarl-MagnusWahlgren
Key Learning Points
Acute extremity compartment syndrome is a surgical emergency associated with
•
signicant morbidity if not expeditiously managed.
• The most important tool in diagnostics is to maintain a high level of clinical
suspicion.
• Patients with classical clinical signs of compartment syndrome do not need any
further investigation, and should undergo urgent fasciotomy.
• Incisions in skin and fascia need to be long enough to make tissues loose and
allow for postoperative swelling.
• After compartment syndrome has resolved, delayed primary closure of the fasci-
otomy incisions is performed, with the intracutaneous suture method
recommended.
20.1 Introduction
Acute extremity compartment syndrome is a surgical emergency associated with
signicant morbidity if not expeditiously managed. It requires prompt diagnosis
and early treatment with compartment decompression for good clinical outcome.
D. Lindström (*)
Section of Vascular Surgery, Department of Surgical Sciences, Uppsala University,
Uppsala, Sweden
e-mail: david.lindstrom@akademiska.se
C.-M. Wahlgren
Department of Vascular Surgery, Karolinska University Hospital and Karolinska Institutet,
Stockholm, Sweden
e-mail: carl.wahlgren@sll.se
R. Fitridge (ed.), Mechanisms of Vascular Disease,
https://doi.org/10.1007/978-3-030-43683-4_20
455© Springer Nature Switzerland AG 2020
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The denition of acute extremity compartment syndrome is an increased pressure within the compartmental space leading to decreased perfusion pressure and
hypoxaemia of the tissues. This may lead to irreversible ischaemic necrosis of the
muscles and nerves in the compartment causing functional impairment, limb amputation, multiple organ failure, or death [1, 2].
Acute limb compartment syndrome (ACS) in vascular surgery is mostly related
to ischemia-reperfusion (I/R) injury associated with acute ischaemia, vascular
trauma, and phlegmasia cerulea dolens [3–5]. Iatrogenic causes with accumulation
of blood or contrast uid within the compartment after catheter/wire perforation
have also been described [3, 4]. Most extremity compartment syndromes result
from internal compartment expansion due to fractures or crush injuries but also
external compression from burns, tight plaster cast or bandage may occur [6]. The
aim of this chapter is to summarise the pathophysiology and management of upper
and lower limb compartment syndromes.
D. Lindström and C.-M. Wahlgren
20.2 Epidemiology
No comprehensive review of the prevalence of extremity compartment syndrome
has been published due to the variation of causes [7]. The incidence of lower extremity compartment syndrome after revascularization of acute ischaemic limbs is
approximately 10–20% [5, 8, 9], but in contrast, the need for fasciotomy after elective vascular surgery is very low, from 0.15 to 0.45% [10]. Patman found that 32%
of extremities with arterial injuries and only 2% with embolic occlusions underwent
fasciotomy. In a retrospective series of vascular surgery patients (107 patients; 113
limbs) undergoing lower extremity fasciotomy, 72% of limbs underwent revascularization for acute limb ischaemia, 6.2% of limbs were related to acute aortic disease,
and 20% of limbs had undergone elective vascular surgery [2]. In total, 57% of
limbs had signs of ACS and a therapeutic fasciotomy was performed, while 43%
fasciotomies were prophylactic. Data from the US National Trauma Data Bank
showed that patients sustaining lower extremity arterial trauma required a fasciotomy in up to 42% of cases [11].
20.3 Pathophysiology
Skeletal muscles, nerves, and vessels in the upper and lower extremities are arranged
into compartments surrounded by fascia. The upper arm contains two compartments
(anterior and posterior) and the forearm has three (volar, lateral, and dorsal) compartments. In the thigh, there are three compartments (anterior, medial, and posterior), whereas there are four in the lower leg (anterior, lateral, deep posterior, and
supercial posterior) [6, 12]. Compartments within the forearm and lower leg are
especially limited in their ability to accommodate tissue oedema and are therefore
Injury to
compar
tension
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Pathophysiology andManagement ofLimb Compartment Syndromes
tment
457
Tissue
Ischemia
Interstitial
edema
Cellular
necrosis
Fig. 20.1 Pathophysiology of acute extremity compartment syndrome [1, 14–16]
Increased
tissue
pressure
Reduced
perfusion
pressure
Venous
hyper
more prone to develop increased compartment pressures [13]. The lower leg is the
most common location of acute extremity compartment syndrome, with the anterior
and lateral compartments most frequently affected [12].
The pathophysiology of acute extremity compartment syndrome involves an
external compression or an internal expansion within the compartment that leads to
increased tissue pressure, reduced capillary blood ow, local tissue hypoxia and
local tissue necrosis (Fig.20.1) [1, 14]. Intrinsic causes of acute extremity compartment syndrome are tissue injury caused by a direct traumatic event or tissue
ischaemia and reperfusion [1, 15]. The most common cause of compartment syndrome in vascular surgery is tissue oedema due to ischaemia-reperfusion injury
caused by limb revascularisation. A traumatic vascular injury is often accompanied
by fractures, so that ischaemia–reperfusion and haematoma formation may both
contribute to the limb compartment syndrome [16]. The rising tissue pressure
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D. Lindström and C.-M. Wahlgren
impairs venous outow by compressing the veins. This increase in venous pressure
reduces the arteriovenous pressure gradient, resulting in diminished local perfusion
[1, 15, 16].
The combination of increased pressure in the interstitial and intercellular uid
spaces shuts off transcapillary movement. The resultant cellular ischaemia leads to
muscle and nerve damage. Interstitial oedema develops from tissue necrosis and
further worsens hypoxaemia and compartmental swelling. During acute limb ischaemia, the combination of decreased oxygen supply and congestion of red blood
cells within the capillaries triggers a complex cascade of metabolic, inammatory,
and prothrombotic pathways [17, 18]. The cell shifts energy metabolism from an
aerobic to anaerobic mechanism, producing lactic acid. Continued ischaemia causes
depletion of energy-rich adenosine triphosphate (ATP), leading to leakage of extracellular calcium into the muscle cells, which ultimately results in dysfunction and
cell death [19].
Reperfusion injury represents the response to tissue injury when the blood ow
is restored after ischaemia. This contributes to a systemic inammatory, metabolic,
and thrombotic response. Microvascular dysfunction mediates many of the local
and systemic consequences of ischaemia-reperfusion injury with a plethora of
changes specic to arterioles, capillaries, and venules [17, 20]. This includes
impaired vasodilation, decreased perfusion and uid leakage, and increased
permeability.
Ischaemia-reperfusion injury leads to microcirculatory changes due to activation
of inammatory mediators. Increased arterial resistance leads to decrease perfusion
in the capillaries. The permeability results in an increased rate of transcapillary uid
leakage. Impaired tissue perfusion and oedema will further raise the intracompartmental pressure [17, 20]. The no-reow phenomenon is another factor in this
response relating to vascular congestion in the arterioles and capillaries [13, 20].
Reactive oxygen species cause damage including injury to DNA, oxidation of fatty
acids and lipids, and oxidation of proteins and co-factors necessary for enzymatic
function [
21]. This leads to capillary leakage, resulting in additional oedema and
rising compartment pressure. (see Chap. 18, Pathophysiology of IschaemiaReperfusion injury).
The duration of ischaemia correlates with the onset of irreversible changes in
various tissue types. The critical ischaemic time in different tissues at normal temperature can be dened as the maximum ischaemic time interval that a tissue can
tolerate and still remain viable [22]. In the extremities, muscle tissue has the highest
risk for ischaemia-reperfusion injury [17].
An ischaemic time of 4–6h predisposes the patient to the development of a compartment syndrome [23]. Large-animal studies have demonstrated the neuromuscular ischaemic threshold of the limb to be less than 5h, and similarly recommended
restoration of ow within 3h of injury for optimal functional recovery. Haemorrhagic
shock also worsens the impact of ischaemia on the neuromuscular structures of the
limb and reduces the ischaemic threshold to as little as 1h [13].
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