A man in his forties with impaired cognitive and circulatory function after a fall

A man in his forties was brought to the trauma unit of a university hospital. According to the information received by the Emergency Medical Communications Centre, he had fallen down a 3–4 m slope, possibly as a result of intoxication. The ambulance team reported both cognitive and circulatory impairment. There was no information to suggest previous illness or a history of substance abuse.

Prior to admission, the man was initially awake and alert. However, his level of consciousness changed rapidly, and he became aggressive and was considered to be psychotic. A police escort was required, and handcuffs had to be used. On the way to the hospital, assistance was requested from the air ambulance doctor, as the patient was showing increasing signs of circulatory failure with tachycardia of up to 120 beats/min and his skin was cold and clammy. He lost consciousness and his respiratory rate slowed to the extent that he required Bag-Valve-Mask ventilation. The final readings in the ambulance showed a systolic blood pressure of 90 mm Hg, pulse of 120 beats/min and SpO₂ of 94 %. His pupils were 4 mm, equal on both sides, and unresponsive to light. The patient arrived at the hospital about one hour after his fall.

On admission, the patient underwent a trauma assessment in line with the Advanced Trauma Life Support (ATLS) principles (1).

When the patient arrived at the trauma unit, his circulation was extremely poor. He was pale and sweaty with cold, clammy skin, and was receiving Bag-Valve-Mask ventilation with an oropharyngeal airway. Pulmonary auscultation revealed faint wheezing sounds bilaterally. The thorax was stable upon palpation. Peripheral oxygen saturation could not be measured. A chest X-ray suggested slight mediastinal widening, but no other visible pathology such as pneumothorax or haemothorax.

Initial cardiac rhythm was sinus tachycardia with a frequency of 140 beats/min, with palpable peripheral pulses. Blood pressure was initially measured at 160/140 mm Hg, but a subsequent measurement showed 75/36 mm Hg. X-rays of the pelvis and long tubular bones provided no evidence of fractures. The man had a large abdominal girth, but a preliminary ultrasound scan (focused assessment with sonography for trauma, FAST) revealed neither free abdominal fluid nor signs of pericardial fluid. The patient was deeply unconscious, with a Glasgow Coma Scale (GCS) score of 4. His pupils were 3 mm in diameter.

Arterial blood gases showed pronounced lactic and respiratory acidosis as well as hyperkalaemia: pH 6.83 (reference range 7.36–7.44), pCO₂ 10.0 kPa (4.5–6.1 kPa), pO₂ 13.5 kPa (11.0–13.0 kPa), HCO₃ 12 mmol/L (22–26 mmol/L), base excess −19.9 mmol/L (0 ± 3.0 mmol/L), Hb 16.0 g/dL (13.4–17 g/dL), sodium 145 mmol/L (137–145 mmol/L), potassium 7.3 mmol/L (3.5–5 mmol/L), lactate 20.0 mmol/L (0.4–1.3 mmol/L), anion gap 30.3 mmol/L, glucose 20.0 mmol/L (4.0–6.0 mmol/L). Tympanic temperature was 37.5 °C.

Transfusion of two units of blood was started in the Emergency Department, but with no improvement in vital parameters.

A chest X-ray showed only a possible mediastinal widening, and the chest was considered a less likely site of bleeding than the abdomen. The pelvis and long tubular bones appeared unscathed. However, the patient was too unstable to undergo trauma CT, and as haemorrhagic shock was suspected, it was decided to transfer him directly to the operating theatre for surgery in accordance with the ATLS principles of trauma management (1).

The patient received ketamine, fentanyl and rocuronium for intubation in the operating theatre. Surgery began 35 minutes after admission. The patient underwent laparotomy, but no bleeding was detected in the abdomen. The surgery took 15 minutes. A bilateral intercostal drain was inserted to aid diagnosis, but revealed no bleeding in the pleural cavities. Supportive care to help stabilise the patient was provided at the same time, including medications and fluids to raise blood pressure, normalise acidosis and lower potassium levels. Fifty-five minutes after admission, a run of ventricular tachycardia occurred along with circulatory collapse requiring advanced cardiopulmonary resuscitation. The acute Extracorporeal Membrane Oxygenation (ECMO) team was summoned to assess the patient's suitability for venoarterial extracorporeal mechanical circulatory support. Return of spontaneous circulation (ROSC) was achieved after approximately 15 minutes, and ECMO was considered not to be indicated. Echocardiography revealed no sign of cardiac tamponade, and suggested a hyperdynamic circulation without regional cardiac dysfunction. A neurosurgeon considered the clinical picture inconsistent with a traumatic brain injury.

The patient's circulation remained extremely poor, and he was given a high-dose noradrenaline infusion plus bolus doses of adrenaline. He had been medicated for intubation, but not for the maintenance of anaesthesia. Transfusion of blood products yielded little improvement. A total of five units of red cells, four units of plasma and two units of platelet concentrate were administered in the course of the first 90 minutes. The patient's lactate level fell briefly from 20 to 10 mmol/L, but quickly rose again. The respiratory acidosis worsened, with pCO₂(a) rising to 15 kPa despite an increase in minute ventilation from the ventilator.

Additional interventions were discussed while the patient was still in the operating theatre. About 80 minutes after admission, it was noted that the patient's skin had become remarkably hot. His temperature had not been continuously monitored up to this point, but his nasal temperature was now found to have risen to 41.3 °C, from 37.5 °C on admission. External cooling with ice packs was started immediately. A central venous cooling catheter was inserted, and temperature control was achieved after the initiation of internal cooling.

Upon transfer from the operating theatre to the intensive care unit three hours after admission, the patient was deeply comatose without sedation. Oxygenation proved extremely challenging and saturation remained below 90 % despite treatment with 100 % oxygen (pO₂(a)/FO₂(I) ratio approximately 7 kPa). In addition to vasodilation, the patient developed increasing heart failure with low cardiac output as revealed by thermodilution (pulse index continuous cardiac output, PiCCO) and an echocardiogram, and required very high doses of noradrenaline and adrenaline. Levosimendan was also tried but with no improvement. It was difficult to keep the mean arterial pressure (MAP) above 60 mm Hg, and there was no improvement in the lactic acidosis.

Another set of blood samples taken 3.5 hours after admission showed extensive rhabdomyolysis with a myoglobin concentration of 163 000 µg/L (< 70 µg/L) and CK of 21 800 U/L (50–400 U/L). The creatinine concentration was 286 µmol/L (60–105 µmol/L), urea 7.9 mmol/L (3.2–8.1 mmol/L) and potassium 4.4 mmol/L (3.5–5.0 mmol/L). His platelet count was 73 · 10⁹/L (145–348 · 10⁹/L), INR 1.4 (0.8–1.2), activated partial thromboplastin time (APTT) > 180 s (30–44 s) and fibrinogen < 0.4 g/L (2.0–4.0 g/L), consistent with consumption coagulopathy. Diffuse bleeding began to occur from the surgical wounds and injection sites, as well as from the mouth, nose and respiratory tract, consistent with disseminated intravascular coagulopathy (DIC). Thromboelastography (TEG) was highly abnormal and revealed an almost complete absence of coagulation.

The patient died while receiving intensive care less than seven hours after arrival at the hospital, with clinical and biochemical status consistent with multi-organ failure.