Anaesthesiology Intensive Therapy, 2011,XLIII,1; 34-37

Haemorrhagic shock complicating acute pancreatitis

*Wiesława Duszyńska1, Małgorzata Lipińska-Gediga1, Paweł Domosławski2, Teresa Kaiser1, Grażyna Durek1, Wiktor Bednarz2

1Department of Anaesthesiology and Intensive Therapy, Medical University of Wrocław

2Department of General, Gastroenterological and Endocrinological Surgery, Medical University of Wrocław

Background. Acute pancreatitis may be accompanied by a number of complications. They include diffuse peritonitis, intra-abdominal and retroperitoneal abscesses, and severe haemorrhage. These complications are the cause of approximately 50% of all deaths in acute pancreatitis. 

Case report.
A 33-year-old man was admitted to ITU with septic shock, due to acute pancreatitis and necrosis after multiple surgeries. On the fifth day after admission, his condition deteriorated due to respiratory distress and massive bleeding from the splenic region requiring surgical packing. On the next day, the bleeding became critical. More than 2000 mL of blood was evacuated from the peritoneal cavity, the bleeding site was re-packed, and the patient was transfused with RBCs, FFP and 0.04 mg kg-1 of recombinant factor VIIa concentrate. This resulted in haemostasis, however the subsequent clinical course was complicated by septic shock, perforation of the transverse colon and peritonitis. The patient eventually recovered and was discharged home after 105 days in hospital. 

Multifactorial management of acute pancreatitis is essential; in cases of severe haemorrhage, surgical packing and administration of recombinant factor VIIa concentrate are key components of successful treatment.

According to the Atlanta classification, severe acute pancreatitis (AP) is characterized by local and/or systemic complications. The severe form of AP affects 15-20% of patients with acute pancreatitis; the mortality rate is 20-40% [1]. Some other authors estimate its mortality at 80% [2]. The most severe systemic complication is septic shock developing during local complications, e.g. pancreatic necrosis, pancreatic abscess, peripancreatic fluid collections, or pancreatic pseudocysts.

Severe AP may be accompanied by clotting disturbances in the form of intravascular coagulation and/or intra-abdominal bleeding caused by impaired continuity of vessels due to the on-going inflammatory process and proteolytic pancreatic enzymes. Haemorrhagic complications account for over 50% of deaths in severe AP. The risk of haemorrhage is substantially higher in cases of pancreatic necrosis (13.5%) compared to pancreatic parenchymal inflammation [4].

Massive haemorrhage is evidenced by the blood loss >150 mL kg-1 or 1.5 mL kg-1 min-1 over ≥20 min, or when the patient requires the transfusion of 100% of circulating blood volume during 24 h or 50% of circulating blood volume during 3 h [5]. The standards of management for haemorrhagic shock recommend surgical haemostasis; if infeasible, packing, supplementary transfusions (packed red blood cells, fresh frozen plasma, cryoprecipitate, platelets), normalization of acid-base balance, maintenance of normothermia are advised [6, 7, 8]. In patients with massive peri-, preoperative or posttraumatic haemorrhage, recombinant activated factor VII (rVIIa) should be considered [6, 7, 8, 9, 10]. Patients in haemorrhagic shock require vigorous therapy of systemic disturbances; the chance of survival usually depends on combined actions of an anaesthesiologist and surgeon.

We present a case of successful therapy of haemorrhagic shock during acute pancreatitis.


A 33-year-old patient diagnosed with acute pancreatitis was hospitalized in a surgical ward of the regional hospital where he underwent two surgeries and was discharged home. Due to deterioration of his general condition and a septic fever, the patient was admitted to the teaching hospital and qualified for surgery. During the first procedure, pus was evacuated from the suprahepatic collection, several interloop abscesses were removed; the peritoneal cavity was washed and drained. On postoperative day 6, abdominal CT was performed, which revealed the enlarged liver, spleen, mesentery lymph nodes and the abscess cavity, 22x15x12 cm, (Fig. 1) involving the pancreatic region, descending posteriorly between the spleen and left kidney towards the pelvis minor, and an inflammatory infiltration in the lumbar-iliac muscle. The patient was scheduled for re-surgery during which about 1.5 L of pus and necrotic tissues were evacuated from the abscess cavity of the pancreatic region descending retroperitoneally to the ili
ac ala. The irrigation drainage of the abscess cavity was applied. 

After surgery, the patient was sent to ITU. On admission, he was conscious, breathed spontaneously (tachypnoe); SpO2 was 98%, SAP/DAP 130/80 mm Hg, HR 95 min-1. Laboratory tests showed: WBC 12 G L-1; Hb 7.5 g dL-1; CRP 205 mg L-1; D-dimers 2460 mg L-1. On day 5, severe sepsis was recognized. Symptoms of respiratory dysfunction and pneumonia requiring mechanical ventilation were observed.  SAP/DAP decreased to 90/50 mm Hg and diuresis <0.5 mL kg-1 h-1. Clotting abnormalities developed – PTT 70.4 s; moreover, CRP was 101 mg L-1 and PCT >2 ng mL-1. According to the Surviving Sepsis Campaign guidelines, a complex resuscitative and therapeutic bundle was implemented, thanks to which arterial pressure was normalized. Due to contraindications, the patient was not qualified for drotrecogin treatment. 

Due to bleeding from the drains placed in the abdominal cavity laparotomy was performed; fragments of necrotic tissues and blood clots from the abscess cavity were evacuated. Since the source of intensive bleeding from the splenic vein region was undetected, “packing” was administered with several surgical towels left at the site of bleeding. Moreover, the fluid collection near the right iliac spine was drained, the peritoneal cavity rinsed with the saline solution and drained.

On day 6, symptoms of haemorrhagic shock developed. SAP/DAP reduced to 75/45 mm Hg and HR increased to 170 min-1, which required vigorous volume replacement and an intravenous infusion of noradrenaline (up to 3.5 mg h-1) to maintain perfusion pressure. On the same day the patient underwent two surgeries: scheduled and emergent due to massive haemorrhage. About 2-3 litres of blood were removed so were clots filling the entire abdominal cavity; tamponade of the abscess cavity was performed (8 towels) to stop the bleeding. In total, the patients was transfused 10 U of packed red blood cells, 14 U of fresh frozen plasma, platelets, and rVIIa factor which was given immediately after surgical tamponade in a bolus of 0.04 mg kg-1. The treatment administered resulted in stabilization of circulation. The values of selected haematological and clotting parameters during bleeding are summarized in Table 1 and blood preparations used – in Table 2.

Three days later, surgical towels were removed from the abdominal cavity. No signs of bleeding were observed. The haematoma was evacuated from the lower abscess cavity. To prevent the risk of further bleeding, 8 bandages were placed again into the abscess cavity and drainage carried out. After the successive 2 days, no features of abscess cavity bleeding were found; all towels were removed from the abdominal cavity, and passive drainage was provided. In the postoperative period, the features of severe sepsis persisted. On day 22, septic shock with peritonitis and ventilation-associated pneumonia was diagnosed.

During the further days (25-53), the peritoneal cavity was repeatedly washed; adhesions were removed, fluid collections in the retroperitoneal space drained. On ITU day 35, suspecting the perforation of the transverse colon, loop ileostomy and transverse colon region drainage were performed. On day 53, the patient`s condition started to improve gradually.

The ITU treatment was continued due to severe sepsis and septic shock, with features of multiorgan failure, leucopaenia (2.5 G L-1), reduced platelet count (30 G L-1) and prothrombin index (40%), without symptoms of active bleeding.

All complications accompanying acute pancreatitis were cured and the patient was discharged home on day 105.


During therapeutic management of massive haemorrhage, simultaneous suitable causal and substitutive therapy is essential. In most cases, causal therapy is associated with surgical intervention (if the source of bleeding can be controlled in such a way) or pharmacological correction of haemostatic abnormalities.

Three elements of substitutive treatment are pivotal: quick replacement of vascular bed volume (fluid transfusion), supplementation of blood morphotic elements and clotting factors (transfusion of packed red blood cells, platelets, fresh frozen plasma and cryoprecipitate) as well as maintenance of perfusion pressure and normothermia (correction of intravascular volume, use of vasoconstricting agents, and warming of fluids) [9, 11, 12, 13]. The organ and tissue perfusion, maintained thanks to that, limits the risk of metabolic acidosis and hypothermia, which enhance coagulopathies primarily initiated by bleeding. 

Body temperature should be maintained at the level similar to the normal values as even its slight decrease results in slowed kinetics of enzymes involved in the process of coagulation [12].

 One of the therapeutic options for massive haemorrhage, especially if standard therapy proves ineffective, is the use of rVIIa [14]. The factor has good pharmacokinetic properties: distribution volume – 8 L and half-life time 2.3 h in bleeding episodes [10, 15, 16]. The efficacy of rVIIa depends on bleeding source control, restoration and maintenance of normothermia, correction of acid-base balance (pH ≥7.2), PTC ≥ 50 G L-1, fibrinogen 0.5-1.0 g L-1, haemotocrit ≥24%. According to the European guidelines, the administration of r VIIa should not substitute or delay the surgical treatment or other methods enabling the control of bleeding source and ought to be used only when the management mentioned is not haemostatically effective [7, 9, 10, 15, 16].

The case described met the definitional requirements of the diagnosis of massive bleeding. The treatment involved rVIIa administered after surgical intervention and when the clotting parameters required in the guidelines were achieved. The 1:1 ratio of transfused packed red blood cells and fresh frozen plasma was crucial for the efficacy of therapy, which was confirmed by stabilization of the cardiovascular system and haemostasis. 

A relevant element of therapeutic management was an appropriate and prompt decision taken by the surgeon to institute surgical treatment. In our case “packing” was applied using surgical towels, which stopped numerous parenchymal bleedings and haemorrhage from the region of or from the splenic vein itself. Packing is the treatment of choice once other methods of surgical bleeding control have failed. Quick control of bleeding and a smaller volume of blood loss are also important during further recovery from haemorrhagic shock.

In the further postoperative period, no acid-base imbalance or features of renal failure were observed. Proper causal and symptomatic treatment decided about effective control of this life-threatening condition and successful further therapy.



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*Wiesława Duszyńska

Katedra i I Klinika Anestezjologii i Intensywnej Terapii
Akademii Medycznej we Wrocławiu
Akademicki Szpital Kliniczny
ul. Borowska 213, Wrocław 50-556

received: 25.05.2010
accepted: 06.08.2010