By Paul Mazurek
An 88-year-old male is awaiting the arrival of a critical care transport team in the Coronary Intensive Care Unit (CICU) of a regional heart and vascular center. The patient is to be transported to an academic teaching center for definitive care. He presented to the emergency department (ED) with a two-day history of progressively worsening dyspnea. His past medical history includes hypertension and high cholesterol. Past surgical history includes endovascular repair of a leaking abdominal aortic aneurysm two days prior to this acute illness.
Upon arrival to the referring ED via ambulance, the patient was dusky in color with a labored respiratory rate of 24 breaths/minute and an oxygen saturation (SpO2) of 81 percent. His heart rate was 124 beats/minute and his blood pressure was 81/56. Following emergent endotracheal intubation and mechanical ventilation, 500 ml of IV crystalloid and a norepinephrine infusion, the patient was taken to the cardiac catheterization lab. The interventional cardiologist chose to immediately take the patient for intervention and not await laboratory results secondary to the patient’s acuity.
The only laboratory derangements noted from those studies drawn in the ED reveal a total white blood cell count of 21,000/ml3, a total creatine phosphokinase (CPK) of 5500 IU/L, a serum pH of 7.15 and a serum lactate of 10.6 mmol/L. Other than pulmonary hypertension, the results of a left and right heart catheterization were unremarkable. Following several unsuccessful attempts at intra-aortic balloon pump placement (IABP), the patient was transported to CICU and the referral center was called.
Upon the transport team’s arrival to the CICU, the patient has an arterial line and a pulmonary artery catheter in place. The patient is receiving mechanical ventilation and lung protective strategies are being utilized. Pulmonary artery catheter numbers include a central venous pressure (CVP) of 18 mmHg, a pulmonary artery pressure (PAP) of 46/23 and a pulmonary capillary wedge pressure (PCWP) of 24. His arterial blood pressure is 90/56 on 20 mcg/min of norepinephrine. Urine output over the last four hours has been 60 ml. A nasogastric tube is in place at low continuous wall suction and clinically, the patient’s abdomen is distended and dull to percussion.
Plan for the transport team per medical direction at the referral center is for stabilization to the best of their ability, rapid transport by air (a 40-minute flight), and immediate delivery to the CVL for IABP placement. The old aphorism, “When you hear hoofbeats, think horses, not zebras” has relevance here. Let’s back up to the start of this case.
A head-scratching predicament
The tense abdomen, absence of elevated cardiac markers, and clean cardiac catheterization provide some evidence of an alternate diagnosis. However, these are vague findings and most paths lead to left ventricular dysfunction. A diagnosis to consider, especially with this patient’s surgical history and evidence of multi-system failure (cardiovascular, pulmonary and renal at a minimum) is Abdominal Compartment Syndrome (ACS).
Typically, mean abdominal compartment pressure is negative to slightly positive (<5 mmHg) based upon pressure changes secondary to respiration. Intra-abdominal hypertension (IAH) exists when this pressure exceeds normal parameters1. IAH is “graded” according to severity as follows2:
• Grade I: IAP 12-15 mmHg
• Grade II: IAP 16-20 mmHg
• Grade III: IAP 21-25 mmHg
• Grade IV: IAP > 25 mmHg
Generally speaking, organ dysfunction begins when sustained IAP exceeds 15 mmHg. ACS is identified when IAH produces dysfunction of one or more organ systems. So how does this happen?
Pathophysiology
Abdominal compartment pressure increasing secondary to several mechanisms causes hypoperfusion to organ systems and ultimately organ dysfunction. Various risk factors / mechanisms include4:
• Capillary leak and aggressive fluid resuscitation (e.g., acidosis, coagulapathy, trauma and severe sepsis)
• Increased abdominal compartment contents (e.g., gastric distention, ileus, tumors, hematomas, enteral feeds)
• Abdominal collections of fluid or air (e.g., peritoneal dialysis, ascities, abdominal infection, pneumo/hemo-peritoneum)
• Reduced compliance in the abdominal wall (e.g., positive pressure ventilation, pneumonia / acute lung injury, abdominal vascular surgery5, increased external pressure such as burns and pneumatic antishock garments)
Effects on the pulmonary system are secondary to compliance issues and loss of lung capacity. Hypoventilatory respiratory failure ensues. As a result of increasing IAP, clinical manifestations will include hypercapnia, hypoxia, and increased minute ventilation requirements with increasing ventilatory pressures.
Cardiac output drops as a result of decreased venous return secondary to compression of the vena cava. Higher intrathoracic pressure compresses the heart, producing reduced stroke volume and reduced ventricular end-diastolic volume. Left- and right-sided preload (i.e., CVP and PCWP) may increase. Cardiac workload increases and compensatory mechanisms will eventually fail.
Reduced urine output is secondary to pre- and intra-renal failure. Reduction in cardiac output results in pre-renal failure. Renal blood flow is reduced in the kidney itself secondary to tissue compression.
Increased IAP causes reduced mesenteric bloodflow, resulting in reduced function, ulceration, and translocation of bacteria, increasing the risk of severe sepsis. Reduced hepatic and portal bloodflow causes reduced lactate clearance, glucose metabolism and regulation of the coagulation cascade.
From a central nervous system perspective, increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP) ensues. This is secondary to increases in central venous pressure (CVP) and intrathoracic pressures. Alterations in level of consciousness and brainstem function result.
Management
Mainstay therapy for a patient suffering from ACS is identification with strong clinical evidence and serial measurements and rapid decompression via paracentesis and/or open laparotomy in order to relieve IAP. As a critical care transport provider, a high index of suspicion, medical palliation, and rapid transport to an appropriate destination is imperative. Measurement of IAP is done either directly with an intraperitoneal catheter attached to a pressure transducer or indirectly. Indirect measurement is the most commonly used form as it is easy and less invasive. Typical points of measurement include the bladder and stomach.
From an air medical perspective, medical management is based on five basic principles3,4:
• Increased abdominal wall compliance: typically done with sedation, analgesia, neuromuscular blockade, and reduction in altitude/cabin altitude
• Gastric and intestinal decompression: gastric tube placement and suctioning, rectal tubes, enemas
• Treatment of capillary leak and maintaining vascular fluid balance: diuresis if stable hemodynamically, isotonic crystalloids or colloids
• Hemodynamic and respiratory support: pharmacologic agents, crystalloids, colloids in order to reverse tissue hypoperfusion, appropriate ventilatory management to reverse hypoxia
Transport to a center with general surgery, interventional radiology. and dialysis capabilities will improve survivability and allow the chance for improvement in end-organ perfusion.
Back to our original case
From an overall patient management perspective, care was not all that dissimilar to the care that being rendered in the referring ICU. What may have saved this patient was the transport clinician’s suspicion of IAH. This suspicion altered the sequence of events this patient’s care at the referral center.
A bladder pressure measuring system was attached to the urinary catheter at the sample port. The drainage tube is clamped immediately distal to the catheter and a predetermined amount of fluid is instilled directly in to the bladder and a pressure transducing system is attached to measure mean IAP. Measured IAP was 32 mmHg.
The patient was packaged and transport began with minimal change in hemodynamic and respiratory parameters. An alert was made en route to the surgical team on call, and the patient was evaluated in the ED by both interventional cardiology and general surgery. It was determined that the patient would receive an emergent laparotomy to relieve IAP before any other intervention would occur.
Relief of the patient’s IAH occurred with an exploratory laparotomy and performance of a colostomy secondary to bowel ischemia. In the intensive care unit (ICU), the patient received swan-guided fluid balance and continuous renal replacement therapy (CRRT). Cardiovascular and respiratory function eventually improved and the patient was discharged two weeks later. His renal function never recovered and he was placed on the renal transplant list and is receiving outpatient dialysis three times per week.
Conclusion
From a transport perspective, treating this patient for cardiogenic shock in a traditional manner probably would not have killed this patient. Not recognizing the underlying problem and a second unneeded trip to the CVL might have. This is yet another situation in which being able to perform a thorough history and physical examination, narrowing down a list of differential diagnoses, and formulating an appropriate treatment plan has benefitted a patient. This is an area where exceptional air medical transport providers excel.
References
1. Bailey J and Shapiro MJ. Abdominal Compartment Syndrome. Crit Care (4). 2000. pp. 23-29.
2. Vidal MG, Weisser JR and Gonzalez F, et. Al. Incidence and clinical Effects of Intra-Abdominal Hypertension in Critically Ill Patients. Crit Care Med 36(6). 2008. pp. 1823-1831.
3. Malbrain ML, Cheatham ML and Kirkpatrick A, et. Al. Results from the International Conference of Experts on Intra-Abdominal Hypertension and Abdominal Compartment Syndrome. Intensive Care Med (32). pp. 1722-1732. 2006.
4. Malbrain ML and De laet IE. Intra-Abdominal Hypertension: Evolving Concepts. Clin Chest Med (30). pp. 45-70. 2009.
5. Makar RR, Badger SA, O’Donnell ME, et. Al. The Effects of Abdominal Compartment Hypertension after Open and Endovascular Repair of a Ruptured Abdominal Aortic Aneurysm. Journal of Vascular Surgery 49(4). pp. 866-872. 2009.
