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We continue our discussion of polytrauma today.

Case: A 68-year-old male pedestrian is struck by a motor vehicle moving at high speeds. He is comatose at the scene, intubated, and transferred to a level I trauma center. He undergoes a diagnostic peritoneal lavage, which returns gross blood and is taken emergently to the operating room. He is discovered to have a damaged spleen, a grade III liver laceration, and a non-expanding pelvic hematoma. He undergoes a splenectomy and packing of his liver injury. Intraoperatively, estimated blood loss was greater than 3 liters. He is noted to be cold and markedly coagulopathic. He is brought to the ICU for continued resuscitation. Over the next 4 hours, ongoing fluid resuscitation and blood transfusion for intermittent hypotension. He becomes oliguric, and his peak inspiratory pressures start to rise into 60's despite decreasing tidal volume and increasing rate. An arterial blood gas is obtained: pH 7.24, pO₂ 50, pCO₂ 55.

1.  What is the pathophysiology of his presentation?
2.  How is the diagnosis made?
3.  What therapeutic intervention is necessary?

病例：男性，68岁，在步行时被一高速行驶的机动车撞伤。现场即处于昏迷状态，给予气管插管后送至Ⅰ级创伤中心。因血流动力学不稳定，给予诊断性腹腔冲洗，冲出大量血液，紧急送往手术室。腹腔探查发现，脾脏损伤、肝脏撕裂分级为Ⅲ级和非进行性盆腔血肿。行脾切除术和肝修补术。术中失血估计大于3升。患者四肢厥冷，并呈显著的凝血紊乱，送入ICU行进一步复苏治疗。此后四小时，持续给予液体复苏并因为间断出现的低血压给予输血治疗。出现少尿，吸气压峰值升至60，虽经降低潮气量和呼吸频率但未改善。动脉血气为：pH7.24，pO₂ 50，pCO₂ 55。

1、  患者所处状况的病理生理？
2、  如何诊断？
3、  需要进行哪些干预治疗？

参考答案：

1、  患者所处状况的病理生理？

当腹腔压力增加到影响循环和组织灌注时导致腹腔间隔室综合征（ACS）。ACS影响很多系统，包括心血管、呼吸、肾脏和胃肠系统。

对心血管系统的影响包括降低心输出量，减少静脉回流。其机制有下腔静脉压力增高、膈肌移位（导致下腔静脉牵拉变形）及全身血管阻力增加。部分心输出量减少可通过输液得到改善。因为胸内压增加，PAOP和CVP也增加。

对肺的影响包括增加胸内压、吸气末压增加，顺应性降低（动、静态）。其机理主要是膈肌抬高压迫肺，导致低氧血症、高碳酸血症和气道压增加。

ACS同样对肾脏造成影响。肾脏的效应包括少尿，可导致急性肾功能衰竭，如果IAH早期得到纠正的话，肾衰竭可以纠正。肾血流减少、肾静脉高压、CO减少和肾血管阻力增加均导致肾功能降低。输尿管梗阻并非相关因素，因为输尿管支架不具保护性。

考虑到原发因素为腹腔不能适应增高的腹压，ACS的胃肠效应最复杂，因为消化道对压力变化最敏感。当腹压在10mmHg时肠系膜血流即受影响。静脉高压和肠水肿加重IAH。对肝脏的作用包括与CO降低相应的肝动脉血流减少，门静脉血流也相应减少。肝脏受压及肝静脉变形进一步增加IAH的有害作用，腹压在10mmHg时即可证实这种变化。乳酸清除率减少增加了乳酸作为肠缺血标志的复杂性。

2、  如何诊断？

ACS的诊断取决于对处于危险中的患者所表现出的症状和体征相互影响的仔细准确判断。腹压可通过直接和间接方法进行测量。直接法包括通过放置于腹腔内的导管（与换能器相连）测量腹膜内压力（如腹腔镜检查）。间接方法包括经皮放置下腔静脉导管、胃内探针和囊内导管（intra-vesicular catheters）。膀胱压力测量为金标准。Foley导管容易放置，且价格低廉，对病人及操作者安全，可容易的应用于危险人群。膀胱为腹膜外器官，与腹内结构有良好的顺应性，因此，腹内压力与膀胱内压平行变化。Foley导管通过引流口处与18号静脉压力管道相连，从而与传感器相连接。传感器校零时与耻骨联合平齐，膀胱注入50ml盐水，呼气末测量压力。

膀胱压力有何意义？当ACS发生时，确切地腹内压可因人而异或同一个体不同时间而不同，因此没有一个确定的压力作为ACS发生的标志。因此，对膀胱内压的解释主要依靠临床表现和压力的变化趋势。

3、  需要进行哪些干预治疗？

降低腹压为治疗措施之一，减压时患者需要有效的液体复苏。临时的闭合技术可阻止ACS的发展。闭合假道、"Bogota"包、真空包装及真空海绵技术都属于闭合技术，可预防ACS的形成。显然，纠正低血压和凝血功能是基本。有创监测在指导液体治疗方面具有积极作用。定期的IAP监测也很有必要，以免腹压再次升高并判断闭合效果。原发性闭合可出现在5-7天时，或在患者病情稳定时出现。

What is the pathophysiology of his presentation?

Abdominal compartment syndrome (ACS) results when increased pressure in the abdominal cavity adversely affects circulation and threatens tissue perfusion. ACS affects a myriad of systems, including the cardiovascular, respiratory, renal, and gastrointestinal systems. Cardiovascular system effects include decreased cardiac output and decreased venous return. A number of mechanisms have been purported to explain this decreased cardiac output, including high inferior vena caval pressure, diaphragmatic deviation that deforms the inferior vena cava as the IVC traverses the crura, and increased systemic vascular resistance. The decreased cardiac output can be partially reversed with infusion of intravenous fluids. Pulmonary artery occlusive pressures and central venous pressures are increased as a reflection of increased intra-thoracic pressure. Pulmonary effects include increased intra-thoracic pressures, increased end-inspiratory pressures, and decreased compliance (dynamic and static). The mechanism is primarily mechanical as the diaphragm is forced higher thus compressing the lungs resulting in hypoxemia, hypercarbia, and increased airway pressures.

The kidneys are not spared by ACS. Renal effects include oliguria that can progress to frank renal failure. This progression is reversible if intra-abdominal hypertension (IAH) is corrected early. Decreased renal blood flow, renal venous hypertension, decreased cardiac output and increased renal vascular resistance all contribute to decreased renal function. Ureteral obstruction is not a factor as ureteral stents are not protective.

Considering that the original problem originates from the inability of the abdominal cavity to accommodate increased pressure, the gastrointestinal effects of ACS are the most profound. The gut is the most sensitive organ to IAH. Mesenteric blood flow is affected at pressures as low as 10 mm Hg. Venous hypertension and intestinal edema worsen IAH. Hepatic effects include decreased hepatic arterial blood flow proportional to the decreased cardiac output. Portal blood flow is similarly diminished. Liver compression and hepatic vein distortion further augment the injurious effect of IAH. Changes can be demonstrated with intra-abdominal pressures as low as 10 mm Hg. Decreased lactate clearance confounds the use of lactate as marker of intestinal ischemia.

How is the diagnosis made?

The diagnosis of ACS depends on the recognition of the constellation of signs and symptoms as well as careful attention to patients who may be at risk. Intra-abdominal pressure may be measured by direct and indirect methods. Direct methods include the measurement of intraperitoneal pressure by a catheter placed in peritoneal cavity connected to a transducer (e.g. laparoscopy). Indirect methods include percutaneously placed inferior venal caval catheters, intra-gastric probes, and intra-vesicular catheters. Bladder measurements are the "gold standard". Foley catheters are easily placed, inexpensive, safe for patient and practitioners, and can readily be applied to "at risk" populations. The urinary bladder is an extra-peritoneal, intra-abdominal structure with a compliant wall. Changes in intraperitoneal pressure parallel changes in intra-luminal bladder pressure. The Foley catheter is connected to a transducer via the aspiration port with an 18 gauge IV and pressure tubing. The transducer is zeroed at the symphysis pubis. The bladder is inflated with 50 ml saline. The pressure is measured at end-expiration.

What is the significance of the measured bladder pressure? The exact intra-abdominal pressure at which ACS develops may vary from patient to patient (or within an individual patient) and is not related to a specific pressure. Interpretation of the measurement of bladder pressure, therefore, depends upon the clinical scenario and trend of the bladder pressures. Many authors recommend decompression of all patients at IAP > 25 mm Hg (34 cm H20) in the absence of ACS. Organ injury occurs well before frank ACS develops.

What therapeutic intervention is necessary?

Abdominal decompression is treatment of choice. Patients may require aggressive fluid resuscitation following decompression. Temporary closure techniques may prevent the development of ACS. Prosthetic mesh closure of fascia, "Bogota" bag, vacuum pack, and vacuum sponge are all closure techniques that may protect against the development of ACS. Obviously, correcting hypothermia and coagulopathy is essential. Invasive monitoring plays a role in guiding appropriate fluid resuscitation. Periodic IAP monitoring also plays a role as recurrent elevation mandates re-exploration and revision of closure. Primary closure can occur at 5 to 7 days, or when the patient is stable.
Question Author: Selwyn O. Rogers, Jr., M.D.

References:

1.  Burch JM, Moore EE, Moore FA, et al. Surg Clin North Am 1996;76:833-42.
2.  Eddy V, Nunn C, Morris JA, Jr. Surg Clin North Am 1997;77:801-12.
3.  Ivatury RR, Diebel L, Porter JM, Simon RJ. Surg Clin North Am 1997;77:783-800.


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