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A 47-year-old woman, with no previous medical problems, presented to the Accident and Emergency department with left shoulder pain following a fall onto her left side from a horse. Physical examination was unremarkable and she was discharged with simple analgesia. However, 2 h later, she re-presented with worsening left shoulder pain, dizziness and mild epigastric discomfort. A new examination revealed blood pressure of 100/60 mm Hg, which dropped to 95/65 mm Hg on standing, a Glasgow Coma Scale score of 15 and pulse of 62 beats/min. She was resuscitated with 2 litres of Hartmann's fluid. A focused assessment with sonography for trauma (FAST) scan of her abdomen was negative. Then, 1 h later she experienced generalised abdominal pain and developed postural hypotension. However she remained bradycardic (heart rate 45–60 beats/min). Repeat examination revealed peritonitis. A further FAST scan showed free fluid in the left hypochondrium. A CT scan demonstrated a complex tear of the spleen, for which she underwent an emergency total splenectomy. Her postoperative recovery was uncomplicated.
Hypovolaemic shock can result from absolute deficiency of blood volume. This is usually compensated for by an increase in heart rate (HR). Currently there is no case report in the literature of significant shock secondary to blunt abdominal trauma associated with bradycardia.
A 47-year-old woman presented to our Accident and Emergency department with left shoulder pain following a fall onto her left side from a horse. She had no previous medical problems, did not take any regular medication and was a non-smoker. On examination her vital signs were as follows: blood pressure (BP) 103/68 mm Hg with no postural drop, HR 54 beats/min, respiratory rate (RR) 14 breaths/min and a Glasgow Coma Scale score of 15. Examination of her left shoulder and abdomen was unremarkable. She was discharged with simple analgesia (cocodamol).
However, 2 h later she re-presented to the department. She had worsening left shoulder pain, dizziness and mild epigastric discomfort. Re-examination was the same as previous, without any postural drop in BP. Arterial blood gas and haematological investigations were unremarkable except for leucocytosis (white cell count (WCC) 17 × 109).
She was resuscitated with 2 litres of Hartmann's fluid. A focused assessment with sonography for trauma (FAST) scan of her abdomen was negative.
Then, 1 h later she experienced generalised abdominal pain and developed postural hypotension with lying and standing BP of 96/65 mm Hg and 80/50 mm Hg, respectively. However she remained bradycardic (HR 45–60 beats/min). A repeat examination revealed epigastric and left hypochondrium tenderness. A repeat FAST scan showed free fluid in the left hypochondrium. An urgent CT scan was arranged, which demonstrated a complex tear of the spleen with intraperitoneal fluid estimated to be approximately 5 litres in volume (Figure 1–4). She was subsequently taken to the operating theatre where these radiological findings were confirmed and she underwent emergency total splenectomy. Her postoperative recovery was uncomplicated and she was discharged from the hospital after 5 days.
Second presentation differential:
The patient's progress was uncomplicated. She was discharged 5 days later with appropriate vaccinations and long-term prophylactic antibiotics.
Hypovolaemic shock secondary to haemorrhage is classified into four stages according to the volume of blood loss and associated physiological responses, change in BP, HR, RR, urine output and mental status. Typically there is increasing tachycardia with progressive hypovolaemia. Often, HR is one of the first parameters to change with increasing blood loss (see table 1).1–3
Between 7% and 28% of patients in hypovolaemic shock present with bradycardia.4 5 Common causes for bradycardia in a patient with shock are medications (such as digitalis or β-blockers) and neurogenic shock. Our patient demonstrated none of these.
Another cause of bradycardia in hypovolaemic shock that has been described in literature is severe periarrest haemorrhage.4 6 This was originally thought to be a poor prognostic indicator in a second phase of biphasic response to haemorrhage or volume loss. The first phase consists of tachycardia and normotension mediated by a baroreceptor mediated reflex, which causes vasoconstriction and cardiac acceleration. The second phase consist of falling BP and bradycardia, which is thought to be due to a vasodepressor and cardiac inhibitory response to a significant loss in volume, usually at least one-third of total blood volume.7 The biphasic pattern of response, was clearly not present in this case, as there was no evidence of the initial tachycardic response.
The occurrence of bradycardia in a patient with acute intra-abdominal haemorrhage may be explained by an increase in the parasympathetic drive. Indeed gradual pooling of blood in the abdominal cavity following trauma can result in stretching or irritation of the intraperitoneal cavity and a vagally stimulated reflex causing bradycardia. This has been seen in patients with penetrating abdominal trauma and in those with intraperitoneal haemorrhage following abdominal surgery.7–11 However, to date there is no report of these findings in patients following blunt abdominal trauma. It has also been shown in animal and experimental studies where reflex bradycardic response to acute haemorrhage is abolished when the vagus nerve is cut or if the muscarine antagonist atropine is concomitantly administered.12 From this we can understand and appreciate that bradycardia following intra-abdominal haemorrhage can be explained by this parasympathetic phenomenon, be it penetrating or blunt injury.
It may well be advantageous to have a bradycardia with significant blood loss. When venous return is reduced, bradycardia will result in a longer diastolic ventricular filling time. This could lead to maintenance or increase of cardiac output by an increase in the stroke volume. Alternatively, increased parasympathetic drive may improve tissue perfusion due to vasodilatation. This protective mechanism is seen in patients with critically reduced venous return. Here, vagally mediated cardiac depressor reflexes are activated by mechanoreceptors in the left ventricle. This has been described in patients with extra-abdominal bleeding.7 13
In progressive hypovolaemia circulatory control is changed. Anatomical distribution and contribution of the components of the autonomic nervous system varies from individual to individual. It is speculated that the parasympathetic tone may have been more prominent in this case. Similarly it may be that the baroreceptors responded inappropriately causing an autonomic dysfunction with the lack of sympathetic drive.
In conclusion, patients with acute haemorrhage may not present with tachycardia. Indeed clinicians must be aware that in patients who present with hypotension and bradycardia (or lack of tachycardia) following blunt abdominal trauma may well be in hypovolaemic shock secondary to haemorrhage.
Competing interests None.
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