Fluid resuscitation and source control in catheter-associated urosepsis
Mrs S is a 72-year-old woman with a history of type 2 diabetes and hypertension, admitted from a care home with fever, confusion and a urine dipstick positive for nitrites. On arrival: temperature 38.9°C, heart rate 118/min, blood pressure 82/48 mmHg, respiratory rate 28/min, SpO2 94% on 4 L/min. She is drowsy but rousable. Lactate 3.6 mmol/L, creatinine 180 µmol/L (baseline 80), platelets 110 × 10^9/L, bilirubin 28 µmol/L, INR 1.4. She has received 30 mL/kg of crystalloid (about 2 L) over the first hour and remains on noradrenaline 0.25 µg/kg/min with MAP 66 mmHg. Central venous pressure is 14 mmHg. She has cold peripheries and mottled knees. Blood and urine cultures have been sent; antibiotics were given at 40 minutes. There is no obvious source other than the urinary tract, and she has a long-term urinary catheter.
1. Assess her fluid status and fluid responsiveness. What would you do next regarding fluids and vasopressors, and why?
Read the worked answer
CVP 14 mmHg is not a reliable measure of fluid responsiveness, especially with cold peripheries and possible vasoplegia. The history of 30 mL/kg (about 2 L) plus noradrenaline 0.25 µg/kg/min and mottled knees suggests she may be both under-resuscitated and receiving too much fluid.
Assess dynamic indices: passive leg raise with stroke volume or pulse pressure change, or stroke volume variation if sinus rhythm and ventilated with adequate tidal volume. Look at lactate trend, capillary refill, urine output, and echocardiography (IVC variability, LV filling, RV function).
Plan:
- If fluid responsive, give a 250–500 mL crystalloid bolus and reassess; do not give further large volumes blindly.
- If not fluid responsive, stop fluids and escalate vasopressors. Start vasopressin (0.03 units/min) if noradrenaline is >0.2–0.3 µg/kg/min, to reduce catecholamine load and pulmonary pressure.
- Target MAP 65 mmHg initially; individualise higher if she has chronic hypertension.
- Avoid starch and large-volume saline; use balanced crystalloid.
The reasoning: excess fluid worsens pulmonary oedema, gut oedema and mortality; vasopressors are not a last resort but part of early haemodynamic support.
2. Discuss the role of hydrocortisone, vasopressin and bicarbonate in this patient, with the evidence that shapes your choice.
Read the worked answer
Hydrocortisone: consider 200 mg/day IV in septic shock with ongoing vasopressor requirement (typically noradrenaline >0.1–0.2 µg/kg/min for >4 h). The ADRENAL and APROCCHSS trials showed faster shock reversal but no clear overall mortality benefit; a subgroup may benefit. Check a random cortisol if there is diagnostic doubt, but do not delay treatment for it.
Vasopressin: add at 0.03 units/min when noradrenaline is escalating, per Surviving Sepsis Campaign guidance. It reduces noradrenaline dose and may reduce atrial fibrillation compared with further catecholamines; no mortality benefit in the VANISH trial.
Bicarbonate: not routinely indicated. It may be considered for pH <7.20 with AKI (BICAR-ICU suggested reduced vasopressor requirement in that subgroup, but no mortality benefit). Calculate her bicarbonate from the blood gas. Do not give bicarbonate simply to normalise a number, and watch for hypernatraemia and fluid overload.
The principle: treat the cause and perfusion, not the surrogate number.
3. She deteriorates with worsening renal function and rising lactate. Source control is discussed. What are the priorities and how would you decide about removing the catheter and imaging?
Read the worked answer
Priorities in suspected urosepsis with a long-term catheter:
- Source control is urgent. Remove or change the catheter; a blocked or colonised catheter is a persistent source.
- Obtain imaging (ultrasound or CT) to exclude obstruction, pyonephrosis or abscess. Obstruction requires decompression (nephrostomy or stent) - antibiotics alone will fail.
- Review cultures: catheter urine cultures are often polymicrobial and may reflect colonisation, so pair with blood cultures and clinical signs. De-escalate antibiotics once sensitivities are known.
- Reassess fluid balance and renal function; avoid nephrotoxins; consider RRT if indications develop.
Decision-making: the patient lacks capacity; the daughter holds lasting power of attorney. Discuss the likely benefits and burdens of drainage and ICU escalation. If obstruction is confirmed, decompression is usually proportionate and reversible. If there is no obstruction and she is deteriorating despite antibiotics, the question shifts to goals of care. Document the discussion and a time-limited trial.