多发伤(part4)【每周一问】NO.77
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发布日期: 2007-04-02 15:13 文章来源: 丁香园
关键词: 多发伤 腹腔间隔室综合征 每周一问 点击次数:


We continue our discussion of polytrauma today.

Case: A 68-year-old male pedestrian is struck by a motor vehicle at high speed. He is comatose at the scene, intubated, and transferred to a level I trauma center. Given hemodynamic instability in the emergency room, he undergoes a diagnostic peritoneal lavage, which returns gross blood. He is taken emergently to the operating room. Upon exploration, 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: pH7.24, pO2 50, pCO2 55.

1.  What is the diagnosis?
2.  What are the clinical signs of this condition?
3.  What are the risk factors for this condition?


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、  诊断?
2、  该情况下的临床表现?
3、  该情况下的危险因素?


参考答案:

1、  诊断?

该病人属于腹腔间隔室综合征。腹内高压(IAH)表示腹腔压力(IAP)显著升高。IAP正常下为0mmHg。当IAP增高导致腹腔脏器出现功能障碍时发生腹腔间隔室综合征,其临床诊断包括:腹部显著膨隆、IAP升高、气道压升高、缺氧与高碳酸血症并存的通气不足、肾功能障碍以及这些情况在腹腔压力降低后得到改善。

Burch提出了一个IAH的分级标准:
Ⅰ级:10-15 mm Hg
Ⅱ级:16-25 mm Hg
Ⅲ级:26-35 mm Hg
Ⅳ级:>35 mm Hg

2、  该情况下的临床表现?

当局限性解剖空间的压力增高到影响循环并威胁组织灌注时,导致间隔综合征发生。发生间隔综合征的确切IAP因人而异。腹腔间隔室综合征临床表现:

  腹部膨胀
  IAP增高
  难治性少尿
  PIP升高
  高碳酸血症
  难治性低氧血症(增加FiO2和PEEP无效)
  难治行代谢性酸中毒
  ICP增加

3、  该情况下的危险因素?

有很多危险因素可影响腹腔间隔室综合征的进展。包括:

  手术后出血
  术后凝血紊乱
  梗阻性肠管扩张
  大的疝气复位后
  腹主动脉动脉瘤破裂
  肝周或腹膜后填塞
  腹腔镜检查
  腹水

What is the diagnosis?

This case presentation is emblematic of a patient with abdominal compartment syndrome. Intra-abdominal hypertension (IAH) represents markedly elevated intra-abdominal pressure (IAP). Normal IAP is 0 mm Hg. Abdominal compartment syndrome occurs when increases in IAP leads to abdominal organ dysfunction. Abdominal compartment syndrome is defined clinically by a tensely distended abdomen, elevated intra-abdominal pressures, elevated peak airway pressures, inadequate ventilation with hypoxia and hypercapnia, disturbed renal function, and improvement of these features after abdominal decompression.

Burch proposed a grading system for IAH.
Grade I : 10-15 mm Hg
Grade II : 16-25 mm Hg
Grade III : 26-35 mm Hg
Grade IV : >35 mm Hg
(Note: 1 mm Hg = 1.36 cm H20)

What are the clinical signs of this condition?

Compartment syndrome results when increased pressure in a confined anatomical space adversely affects circulation and threatens tissue perfusion. The exact IAP at which this takes place may vary from patient to patient (or within an individual patient) and is not related to a specific pressure. Clinical signs of abdominal compartment syndrome include the following:

•  Abdominal distention
•  Increased IAP
•  Oliguria refractory to volume administration
•  Increased PIP
•  Hypercarbia
•  Hypoxemia refractory to increasing FiO2 and PEEP
•  Refractory metabolic acidosis
•  Increased ICP

What are the risk factors for this condition?

There are a number of risk factors for the development of the abdominal compartment syndrome. The following represents a list of factors, which may contribute to the development of this syndrome:

•  Postoperative hemorrhage
•  Postoperative coagulopathy
•  Bowel distention from obstruction
•  Reduction into the peritoneal cavity of large hernias
•  Ruptured abdominal aortic aneurysm
•  Excessive crystalloid resuscitation
•  Perihepatic or retroperitoneal packing
•  Laparoscopy
•  Ascites

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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