Compartment Syndrome ofthe Abdominal Cavity

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concemed about the "enormous pressure increase that often precluded ... Hypertension, below, is preferred because it guides therapy. ... It usually requires op ..... also be an increased risk for infection. ... first because abdominal veins are emptied upon sudden in crease in .... Xl. Surgical Problems in the Intensive Care Unit.


1888

1 71. Compartment Syndrome

of the Abdominal Cavity Dietmar H. Wittmann

Introduction CAVITY IS A COMPARTMENT. The THE ABDOMINAL CAVlTY abdominal cavity may be considered as a single compartment with a containing wall of limited compliance. It responds to hypervolume increase of any of its contents with abdominal hyper­ protension. Elevated intraabdominal pressure (lAP) may pro­ foundly impair physiology and organ func1ion. Once a critical threshold volume is reached, relatively small increments of augvolume are associated with relatively enormous pressure aug­ mentations that quickly lead to decompensation (Figs 171-1, [11. Excessively increased lAP may result in 171-2, and 171-3) [n total loss of function and may lead to death.

HISTORY. In 1911 Emerson [2J introduced his readers to a series of elegant experiments with the statement that "pressure conditions which exist within the peritoneal cavity" had re­ received insufficient ;ltrention. attention. Not much has changed since, and topic is not covered in current textbooks of surgery or the topiC critical care. As early as 1876, Wendt [3J discussed the reduced urinary flow in the presence of abdominal hypertension. When

surgeons started treating peritonitis pentonltls operatively, they were concerned concemed about the "enormous pressure increase that often [4l. precluded abdominal closure" [4]. In subsequent years, the topic was subject to ra excellent reviews [5-101, and since 1959, numerous authors described the negative effects of abdominal hypertension on the function [2,6-9,11-15l. We learned that of almost any organ system [2,6-9,11-15]. pulmoincreased lAP may also deeply impair cardiovascular, pulmo­ nary, hepatic, and even central nervous system function and may reduce perfusion to the gut and its organs [15-23]. Companment-induced impaired intestinal perfusion may be a critical facrar factor in anastomotic healing. It probably plays a role in many organ dysfunctions that are unsatisfactorily explained. explained cholecystitis. or Examples may be colon ischemia, acalculous cholecystitis, ischemiC bowel. pancreatitis and some forms of ischemic Meanwhile, abdominal hypertension and the abdominal pathocompartment syndrome are recognized as independent patho­ logic conditions from various causes that may lead to dysfunc­ dysfunction of physiology [7,8,24-291. This chapter presents current knowledge about the causes, consequences, and treatment options of intraabdominal hypertension.

Definitions compartThe current literature uses terms such as abdominal compart­ hypenenment syndrome (ACS) [24,26-28,30,311, abdominal hypenen­ sion [32-341, and increased lAP. Whereas the term "ACS" acknowledges the abdominal cavity as a closed space and "syndrome" addresses the associated pathology, the term "abdominal hypertension" is less precise and simply denotes pressure increases above normal. Definitions used in this chapter are listed below. Of the various grading systems proposed, the simple grading system listed in Abdominal Hypertension, below, is preferred because it guides therapy.

COMPARTMENT SYNDROMES IN GENERAL. A compartcompart­ ment syndrome is a condition in which increased pressure in a confined anatomic space adversely affects the function and viability of the tissues therein. Confined anatomic spaces mostly associated with compartment syndromes are the fascial spaces of the extremities, the orbital globe (glaucoma), the cranial cavity (epidural/subdural hematoma), and the kidney capsule (post (postischemic ischemic oliguria). Protmded bowel in abdominal compartment syndrome. Fig. 171-1. Protntded after laparot­ laparotThere is massive abdominal edema in a trauma patient afrer omy and fluid resuscitation for hemorrhagic shock. The abdominal content is covered with the artificial burr [106,109J. [106,1091. Although each coment em wide, almost the width of both sheet of the artificial burr is 30 cm sheets combined was required to cover all the protruded bowel and mush rooms omentum. The hook sheet consists of polypropylene micro micromushrooms that cling into a white loop sheet consisting of a meshwork of polyamide and polypropylene loops. Please see Colur Color Plale Plate 171-1

_

--._

.

SYNDROME, ACS is a ABDOMINAL COMPARTMENT SYNDROME. condition in which sustained increased pressure within the abdominal wall, pelvis, diaphragm, and the retroperitoneum adversely affects the function of the entire gastrointestinal tract extra peritoneal organs. It usually requires op­ opand connected extraperironeal erative decompression.

171. Compartment Syndrome of the Abdominal Cavity

12 ~5

10 41 :" • _ \.

-x-

--." ~ ... - • • "2S

- ~- WP (mm Hg)

-+

'MPAP (mm Hg)

---to-- MAP (mm Hg) ~MAP(mmHg)

·····6 ..··HR (beat/min) (beaUmin) ·····A",,·HR

0 ! 0

20

10

30

40

50

Intra-abdominal Pressure (mm Hg)

60

70

80

Fig. Fig 171- 7. Hemodynamic changes If II [50].

PreTable 171-3, Hemodynamic Variables Pre­ (lAP (lAP

= 49 = 19

± 11 II Torr) and Postdecompression :!: ± 7 Torr) in 11 Trauma Patients :!:

VariabJe

Unit

Hean Heart rate Mean arterial pressure Pulmonary artery occlusion pressure Central venous pressure Cardiac index Stroke volume index Right ventricular ejection fraction Right ventricular end-diastolic volume Right ventricular end-diastolic compliance Systemic vascu vascular lar resistance index

beats/min mm Hg (Torr) mmHg

Pre

Post

p

± 18 124 :!: 102 :!: ± 18

± 15 107 :!: 104 :!: ± 20

30 :!: ± 11

± 6.3 24 :!:

09

Torr

29 :!: ± 12

21 :!: ± 7.2

06

Llmin/m'2 Llmin/m mllm' mUm 2

3.7::': 37 :!: 0.6 0,6 30 ± 8.0 30:!:

0,8 ± 0.8 3.9 :!: 37 ± 10 37:!:

.44 .08 08

%

37 ± :!: 95

34 ± :!: 73

.48

2 mllm mUm

83:!: 83 ± 18

110 ± :!: 24

.01

2

mllm Torr mUm

dyne cm- 5 sec/m 2

lAP, intraabdominal pressure. From ref. 34, 34. with permission. pennission.

36 ± 2.1 36:!:

1,634 ± 474 ] ,634 :!:

005 .71

5.9 :!: ± 2.4

01

1,874 :!: ±863 863

.23

[l6,77] or rise [16,77,78] [16,77,78] The direction of although it may fall [16,77) hyperresponse is influenced by the degree of inrraabdominaJ intraabdominaJ hyper­ tension and other compounding factors discussed below. below, common response to elevated IAP, LAP, compen­ compenTachycardia is the conunon sating for the decrease in stroke volume to maintain cardiac [18,50,62,77] output [18,50,62,77].

Increased Systemic Vascular Resistance. The mechanisms of the increase in vascular resistance have not been elucidated to be due to mechanical compression of capillary but are likely to beds or reactive nitric oxide deficiency [1,17,21,23,37,43,51, 53,62,63,77.78] 53,62,63,77,78J. Effects on Cardiovascular Monitoring. Increased lAP mod­ modifies various commonly monitored cardiovascular parameters. parameters, pressure, central venous pressure. pressure, pulmonary Femoral vein pressure. capillary wedge pressure, and right atrial pressure increase 16, 19,21 ,22,37,43, disproportionately with increasing lAP [l, [1,16,19,21,22,37,43, 48,50,53,56,57,68,76]. 48,50,53,56,57,68,76J.

RESPIRATORY FUNCTION Atelectasis and Pneumonia. Both hemidiaphragms are pushed upward because of increased lAP, decreasing thoracic volume and compliance [21,57,86], Decreased volume within the pleural cavities is predisposed to atelectasis and decreases alveolar clearance. Pulmonary infections may resulr. result. PneumoPneumo­ nia is a typical early complication in abdominal hypertension [87J. from diffuse peritonitis [87]. patients Ventilation and Respiratory Failure. Ventilated paliento with abdominal hypertension require increased airway pres­ pressure to deliver a fixed tidal volume [l6,19,22,30,57J. [16,19,22,30,57]. Protrusion of the diaphragms into the pleural cavities raises intrathoracic pulmopressure, depressing cardiac output and augmenting pulmo­ [50J. Ventilation/perfusion abnormalinary vascular resistance [50]. abnormali­

171. Compartment Syndrome of the Abdominal Cavity

1895

40 35

-.::......

30

...CIl

25

~

~





y = 6E-05x

22._ 2

0.1368x + 83.762

R = 0.9903

Q)

::l ::::l

rJl C/l rJl C/l

...CIl

20

roc: 'E 'E

15

Q)

Q. c.

(ij

0 "0

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"...

«I III

.E .5

10 5 0 400

500

600

700

800

900

1000

1100

1200

Inferior Vena Cava Flow (mllmin) (ml/min)

Fig. 171- 8. Inferior vena cava flow in cwo dogs [49].

(JAP = 49 :!: (JAP = 19 :!: Table 171- 4, 4. Pulmonary Function Variables Pre- (lAP :': 11 Torr) and Postdecompression (lAP :': 7 Torr) in 11 Trauma Patients \'"riable

Unit

PaUl (partial pressure of oxygen in arterial Pau, anerial blood) [':teo arterial blood) I'aeo z (partial (panial pressure of carbon dioxide in anerial Fio L (fraction of inspired oxygen) Pao/Fio Paoz/Fio z Q/Q, Q1/Q, (intrapulmonary shunt shum fraction) Peak inspiratory pressure Positive end-expiratory pressure Tv (tidal volume) Cdyn (dynamic compliance)

Torr Torr Ofo %

Pre

80 ± 36 35:!: 35:': 8.3 54:!: 24 54:': :': 78 165 :!:

Ofo % cm H HzO 20 cm H HzO 20 ml ml/cm H 2 0

33 ± 12 65 ± 7.5 20:!: 20:': 91 552:!:171 552:':171

13 ± 5.0

p

Post 124 :!: :': 34 :!: 34:': 53:!: 53:': 236:!: 236:': :!: 21 :': 46:!: 46:': 18 :!: ~ :!: 638 :':

82 99 18 119 12 12 9.5 95 133

24 ± 6.8

.04 76 .84 03 .04