Al-Nammari S1, Yae-Eun Suh2 and Roberton BJ3
1Orthopaedics & General Surgery SHO Southern General Hospital, Glasgow shafic2@doctors.org.uk
2Cardiology SHO St Thomas’ Hospital London yaeeun@hotmail.com
3Cardiology SHO St Thomas’ Hospital London benroberton@hotmail.com
SMJ 2006 51(2): 54
Abstract
A major complication of thrombolytic therapy is haemorrhage. A case of intraperitoneal haemorrhage necessitating three laparotomies is described in a patient following thrombolysis. This is the only documented case of a non-hepatic intraperitoneal haemorrhage occurring post thrombolysis in a patient without risk factors and without a hepatic source being identified. Retroperitoneal haemorrhage1 and intraperitoneal haemorrhage from a hepatic source have previously been described2,3,4.
Keywords: Thrombolysis, Tenecteplase, Complication, Laparotomy, Haemoperitoneum.
A major complication of thrombolytic therapy is haemorrhage. A case of intraperitoneal haemorrhage necessitating three laparotomies is described in a patient following thrombolysis. This is the only documented case of a non-hepatic intraperitoneal haemorrhage occurring post thrombolysis in a patient without risk factors and without a hepatic source being identified. Retroperitoneal haemorrhage1 and intraperitoneal haemorrhage from a hepatic source have previously been described2,3,4.
A thirty five year old male presented to a GP led hospital with a two hour history of epigastric and chest pain that was ischaemic in nature. There was no previous cardiac or GI history of note. On arrival ECG showed ST segment elevation of 1.5mm in leads I and AVL with reciprocal ST depression of 1mm in leads III and AVF. He was diagnosed with an Acute Anterior Myocardial Infarction and was thrombolysed with Tenecteplase. He concurrently received aspirin, diamorphine and clexane. The patient was transferred to our inner city A&E by fixed wing aircraft for further management and arrived three hours post thrombolysis. He had been pain free and haemodynamically stable throughout transfer but on arrival he was complaining of dizziness without palpitations and generalised lower abdominal pain. On examination he was haemodynamically unstable (HR 120bpm, BP 70/60mmHg). There were no signs of cardiac tamponade or anaphylaxis. His abdomen was diffusely tender with guarding and absent bowel sounds. Repeat ECG was consistent with myocardial reperfusion and ECHO showed only minimal left ventricular impairment with no pericardial fluid. Abdominal ultrasound demonstrated massive intra-abdominal free fluid. No source for the intra-abdominal haemorrhage was identified. Haemoglobin and clotting were normal.
At this point all anticoagulant, anti-platelet and thrombolytic agents were stopped. The patient was resuscitated in A&E with mixed crystalloid and blood; and was taken to theatre when haemodynamically stable. Emergency laparotomy five hours post thrombolysis revealed three litres of fresh intraperitoneal blood and clot within both the greater and lesser sacs. No active bleeding was identified, and the liver was entirely normal. A dilated short gastric vessel with a small blister was noted. There was no active bleeding from this point but the vessel was clipped empirically. Four hours postoperatively the patient again became haemodynamically unstable (HR 115bpm, BP70/55 mmHg) with a haemoglobin of 6.9g/dL and a normal coagulation screen. Abdominal CT showed a large volume of intra-abdominal free fluid and post laparotomy gas (Figure 1). The patient was returned to theatre and two litres of fresh intraperitoneal blood and clot was found without an identifiable source. The lesser sac and splenic flexure were packed with gauze and the patient received a further blood transfusion. Mesenteric angiography performed the next day did not reveal a bleeding point.
Clexane
and aspirin were restarted four days after the initial haemorrhage without
complication. The patient however
remained on ITU for six more days as he developed a Lower Respiratory Tract
Infection and moderate left ventricular failure as revealed by repeat ECHO for
which he required ventilatory support. Following
this the patient was transferred to the cardiac unit where he made good progress
and was discharged home with no further complications.
This case serves to highlight the importance of occult haemorrhage as a
cause of hypotension in the thrombolysed patients.
References
1. Yap LB, Augustine DX, Kurbaan AS, et al. Retroperitoneal haemorrhage following thrombolyis. Heart 2004; 90; 564.
2. Roongsritong C, Buell JC. Spontaneous hepatic haemorrhage following treatment with tissue plasminogen activator. International Journal of Cardiology 1994; 46: 182.
3. Garcia-Jimenez A, Mao MC MD, Moan DF, et al. Hepatic bleeding and haemorrhagic shock following thrombolytic therapy in patients with acute myocardial infarction. Chest 1997; 111(6): 1787.
4. Ismail A, Cole JP. Subcapsular hepatic and intraperitoneal bleed after administration of tissue plasminogen activator in a patient with acute myocardial infarction. Heart Disease 2000; 2(1); 13-15.