Septic shock after laparotomy for perforated diverticulitis
A 72-year-old woman (60 kg) is admitted with septic shock from perforated diverticulitis. She underwent emergency laparotomy and sigmoid colectomy 12 hours ago. She is intubated and sedated. Norepinephrine is running at 0.45 µg/kg/min to maintain MAP 62 mmHg. Heart rate 112/min in sinus rhythm, CVP 15 mmHg, ScvO₂ 76%, lactate 6.8 mmol/L, urine output 0.2 mL/kg/h for the last 3 hours. She has received 30 mL/kg crystalloid, broad-spectrum antibiotics, and hydrocortisone 200 mg/day. Haemoglobin 88 g/L, platelets 45 ×10⁹/L, creatinine 220 µmol/L (baseline 80), bilirubin 40 µmol/L, INR 1.6. Bedside echocardiography shows a hyperdynamic left ventricle with end-diastolic area 12 cm², no pericardial effusion, and a small inferior vena cava that collapses more than 50% with inspiration. There is no active bleeding. The abdominal wound is clean but the fascia is not closed.
1. Is this patient fluid responsive, and what is your next haemodynamic step?
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The CVP is 15 mmHg, which is not reliably predictive of fluid responsiveness. The collapsing inferior vena cava and hyperdynamic ventricle suggest that she may still be fluid responsive, but the high norepinephrine dose and low urine output mean that indiscriminate fluid loading could worsen oedema without improving perfusion. I would perform a passive leg raise or a 250 mL crystalloid challenge with a stroke volume or cardiac output assessment; an increase of more than 10% indicates fluid responsiveness.
If responsive, give 250 mL crystalloid and reassess. If not responsive, stop fluid loading and start vasopressin 0.03 U/min while continuing norepinephrine, aiming for MAP at least 65 mmHg. Vasopressin may reduce the norepinephrine requirement and is appropriate in catecholamine-resistant septic shock. Consider adding an inotrope only if echocardiography shows impaired contractility, which is not the case here.
The lactate of 6.8 mmol/L and urine output of 0.2 mL/kg/h indicate poor perfusion, but the answer is not more fluid by default; it is a dynamic assessment followed by vasopressor optimisation.
2. What are the priorities for source control and management of the coagulopathy?
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The priority is to exclude an ongoing abdominal source. The fascia is not closed, the wound is clean, but she remains in high-dose vasopressor-dependent shock with a rising lactate. I would discuss urgent return to theatre with the surgical team for washout and reassessment, and obtain cross-sectional imaging only if it will not delay source control.
Coagulopathy: platelets 45 ×10⁹/L, INR 1.6, and no active bleeding. I would not transfuse platelets or fresh frozen plasma purely to correct numbers. If she needs laparotomy, I would aim for platelets above 50 ×10⁹/L and correct fibrinogen or INR only if there is bleeding or an invasive procedure with a high risk of haemorrhage. Vitamin K can be considered if there is evidence of vitamin K deficiency or liver dysfunction. Avoid NSAIDs and other antiplatelet drugs. Monitor platelets, fibrinogen, and bleeding at the wound and drain sites.
3. When would you initiate renal replacement therapy in this patient?
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Renal replacement therapy is indicated for refractory acidosis, hyperkalaemia, pulmonary oedema, uraemic complications, or a toxin that is dialysable, not for a creatinine value alone. This patient has acute kidney injury with creatinine 220 µmol/L and oliguria, but she is haemodynamically unstable and has septic shock; the decision should be based on the trajectory and complications.
I would start continuous renal replacement therapy if she develops refractory metabolic acidosis with pH below 7.2, hyperkalaemia above 6.5 mmol/L despite treatment, fluid overload with impaired oxygenation, or uraemic encephalopathy/pericarditis. In the absence of these, I would continue close monitoring and avoid early initiation purely because of oliguria. If she remains anuric with worsening acidosis despite vasopressor optimisation, CRRT is reasonable. The circuit should be anticoagulated with citrate if there is no liver failure, or with heparin if citrate is contraindicated; the bleeding risk from thrombocytopenia must be weighed.