A 50-year-old Caucasian male, was retrieved from a regional hospital to our tertiary trauma centre following a high velocity motor vehicle crash. Prior to his retrieval he had undergone damage control surgery, including a resuscitative laparotomy, and fixation of limb fractures. He had received a massive haemorrhage protocol (MHP) as part of a red blanket protocol. His presenting injuries at the time included: small volume intracranial haemorrhage and major limb fractures (the cause for his refractory shock in retrospect). There was no spinal injury and no major intrathoracic, intra-abdominal or pelvic injuries. His injury severity score (ISS) was 35. The extent of his lower limb injuries, large volume MTP including tranexamic acid and immobility placed him at high risk of venous thrombosis. His thrombotic risk was balanced against the presence of intracranial haemorrhage and under guidance of Neurosurgery prophylactic heparin was not commenced until after an unchanged day five CT of the head. His Intensive Care Unit (ICU) admission was complicated by delirium and extensive deep vein thrombus (clot burden in both upper and lower limbs). He was discharged from the ICU on day 14 having been commenced on therapeutic enoxaparin, he sustained a PEA cardiac arrest the same day. In the setting of acute deterioration and known extensive clot burden he was presumptively thrombolysed for PE.
A Computed Tomography Pulmonary angiogram (CTPA) and contrast Computed Tomography (CT) abdomen shortly after his cardiac arrest and thrombolysis revealed mesenteric haemorrhage and a large retroperitoneal haematoma in the pararenal space, likely a complication of the thrombolysis. There were no PE identified on the study. His superior mesenteric artery was emergently embolised and the retroperitoneal haematoma managed conservatively. Following the resuscitative phase of his readmission his clinical status improved now some 30 days following his initial presentation. This was punctuated by a slow ventilator wean, unexplained sinus tachycardia, critical illness myopathy, poor oral intake and an agitated delirium. On follow up contrast CT of the abdomen the haematoma measured 22 x 8 x 23 (TV x AP x CC) cm and had no interval change on subsequent imaging.
Poor oral intake had been problematic for this patient. With the importance of protein energy intake in a hypermetabolic post-trauma state nasogastric tube (NGT) was placed to supplement calories. The NGT fell victim to the patient’s delirium on multiple occasions and replacement proved difficult, requiring endoscopic placement and periods where he was NGT free. Twenty-five days into his second ICU stay and 55 days post initial trauma, he was noted to have a large gastric bubble and an NGT was replaced and again promptly removed by the patient. In the early morning of the 26th day he was noted to have ST elevation suggestive of inferior myocardial infarction, most suggestive of right coronary artery territory (with both inferior and right ventricular pattern of change)- (Fig. 2).
Delirium made assessment for chest pain difficult with the patient becoming increasingly agitated. Aside from his sinus tachycardia, his blood pressure and mean arterial pressure (MAP) were initially within normal range and he had no clinical evidence of heart failure. A loading dose of 300mg of aspirin was administered whilst awaiting serial high sensitivity troponin (hsTNI), which were subsequently negative. Full blood count and electrolytes were all within normal range. His Electrocardiogram (ECG) evolved much like inferior myocardial infarction pattern (complicated by right ventricular involvement) over the next 2 hrs as shown in Figs. 3 and 4.
During this time a worsening bradycardia evolved with progressive haemodynamic instability. The patient became less alert, with episodes of profound hypotension (MAP as low as 30mmHg). An adrenaline infusion was rapidly up-titrated as differentials were considered.
An urgent CT with contrast of the abdomen was performed along with transthoracic echo (TTE) undertaken by the cardiology service.
Contrast CT revealed interval increase in the size of the haematoma, compression of D3 (distal duodenum) and resultant gastric distension causing left ventricular distortion (figure 5).
TTE confirmed retrocardiac compression as a result of the expanding retroperitoneal haematoma (figure 6 and 7).
The above findings were presented in a group setting to staff specialists from Intensive Care, Trauma, Cardiology, Interventional Radiology and Cardiac Anaesthetics. An explanation for the patient’s deterioration thought most likely to be a result of:
…the combined mass effect of the haematoma and gastric bubble resulting in a STEMI mimic. Additionally, there was haemodynamic compromise through extra-cardiac compression- “pseudo-tamponade”, and impaired venous return from vena caval compression by the haematoma…
The haematoma was rapidly drained by the Interventional Radiologist yielding more than 1500mL of liquefied haematoma at insertion. This resulted in a return to normal sinus rhythm, no further ECG changes and a swift resolution of shock. A later coronary angiogram showed no stenotic lesions removing the possibility of coronary artery disease contributing to the pathophysiology.