Septic Shower

MET Call Criteria

Call MET immediately if any of the following are present:

🫁 Airway & Breathing

• Airway threatened
• RR <5 or >30 breaths/min
• SpO₂ <90% on supplemental oxygen

🫀 Circulation

• HR <40 or >140 bpm
• SBP <90 mmHg

🧠 Neurology

• Sudden fall in GCS >2 points
• Repeated or prolonged seizures

⚠️ Clinical Concern

• You are seriously concerned about the patient

Nursing Steps — While Waiting for MET

Call MET immediately if criteria are met, then:

1. Stay with the patient — do not leave unattended
2. Oxygen — apply high-flow O₂ via Hudson mask (10–15 L/min); target SpO₂ >94%
3. IV access — confirm patent IV access; establish ×2 large-bore peripheral cannulas if not already in situ
4. Continuous obs — HR, BP (every 5 min), SpO₂, RR, temperature, GCS
5. Blood cultures — collect ×2 sets from 2 separate sites before antibiotics if at all possible
6. Bloods — FBE, UEC, LFT, coagulation, lactate, CRP
7. IV fluids — prepare 500 mL 0.9% NaCl bolus; commence if SBP <90 mmHg or as directed
8. Warmth — warm blankets for rigors; avoid direct heat sources
9. Urinary catheter — insert for strict fluid balance if instructed; monitor urine output closely
10. Document — record time of onset, all vital signs, and every intervention with timestamps
11. Brief the MET team on arrival — allergies, current medications, recent procedures, IV access sites, implanted devices (e.g. pacemaker, biliary stent)

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Why “Shower”? §

The word itself is the clue. A septic shower isn’t a slow build. It’s a sudden drenching wave of bacteria spilling into the bloodstream, hitting the body all at once.

Picture a sewer line that’s been quietly colonised with bacteria for months, sitting behind a one-way valve. Knock that valve open with a catheter and the whole content of the pipe blows back into the system at once. That’s the moment. Within minutes the patient is shaking, spiking a fever, and their blood pressure is dropping.

In IR this comes up more than you’d think, because so many of the procedures involve instrumenting systems that are already infected: bile ducts, abscesses, obstructed kidneys. The act of getting the catheter in is what releases the bacteria.

The same term gets used in a slightly different sense for septic emboli: small fragments of infected clot that break off an infected heart valve (endocarditis) and travel to the lungs, brain, or kidneys. Same idea of “showering” infectious material through the circulation, just via solid debris rather than free bacteria.

What’s Worth Noticing in the Room §

Once you’ve seen one, you’ll spot the early signs before the obs catch up.

The first thing is usually rigors: uncontrollable shaking, the kind where the patient’s teeth chatter and the trolley rattles. Not a shiver. Real, violent shaking that the patient can’t stop. The temperature is climbing fast, often past 39°C. Heart rate jumps over 100, breathing speeds up, and the skin goes either flushed and sweaty or mottled and grey-looking, depending on how far things have moved.

In an older patient the first clue might be none of the above. They just stop making sense. New confusion in an elderly patient post-procedure is sepsis until proven otherwise.

The thing to watch closest is the blood pressure

Sepsis-driven hypotension drops fast. A systolic under 90 is the line where things have crossed into territory that needs vasopressors (drugs like noradrenaline to push the blood pressure back up) and intensive support.

The classic timing after a biliary case is a spike at 30 to 45 minutes post-procedure. If you’re keeping an eye on a recovery patient who’s had a PTC or biliary drain change, that’s the window where you want eyes on them.

Where This Comes Up in IR §

The pattern keeps repeating: an infected fluid-filled space gets manipulated, and the manipulation pushes bacteria into the bloodstream.

Biliary work is the classic. Bile is colonised with bacteria in nearly every patient who’s had a previous biliary intervention, and almost universally in patients with obstructed bile ducts. ERCP (the scope-up-the-duodenum version), PTC (percutaneous transhepatic cholangiogram, going in through the skin and liver to reach the bile ducts), biliary drain insertions, and drain exchanges. Every one of these can set off a septic shower. Prophylactic antibiotics before the case help, but they don’t eliminate it.

Abscess drainage is another. You’re literally puncturing a bag of pus. The act of getting the drain in releases some of that organism load into the circulation, even when the procedure goes perfectly.

Nephrostomy insertion carries the same risk when the kidney’s drainage is obstructed by infected urine. The moment the obstruction is relieved, bacteria can flush back into the bloodstream.

Hepatic embolisation (TACE, SIRTEX) shows up here because the dying tumour tissue can get infected in the days after the procedure and seed the bloodstream from there. Usually a delayed presentation rather than on-table. Uterine fibroid embolisation carries a small but recognised risk for the same reason.

Anything involving an existing central line or PICC is a separate, ongoing pathway. Those lines can be colonised long after they’ve been put in, and a small manipulation (flushing, drawing bloods, exchanging the line) can shower bacteria off the catheter and into the circulation.

Why the Body Reacts So Hard §

The drama is less about the bacteria themselves and more about the body’s response to them.

Gram-negative bacteria, the kind that live in the gut, bile, and urinary tract, carry a molecule called lipopolysaccharide (LPS) in their outer wall. When the bacteria die or fragment in the bloodstream, LPS is released, and it’s about the most provocative signal the immune system has.

A useful way to think about it: imagine setting off every fire alarm in a building at once. The alarms themselves aren’t dangerous. But the response to them, with everyone running, sprinklers firing, fire doors slamming shut, can do more damage than the fire itself. That’s what’s happening physiologically. The body floods the system with inflammatory signals, blood vessels leak, clotting cascades fire off, blood pressure drops, organs start to misbehave.

Left untreated this slides into septic shock and multi-organ failure. The mortality on that progression is brutal. A patient who’s just spiking a fever after a biliary case has a very different outlook to one whose lactate has climbed past 2 and whose blood pressure won’t hold without noradrenaline.

Sepsis vs Septic Shock §

Worth knowing where the line sits, because the management changes once you cross it.

	Sepsis	Septic Shock
What it means	Organ dysfunction from the body’s overreaction to infection	Sepsis + needing vasopressors to keep MAP ≥65 mmHg, and lactate above 2 mmol/L despite fluids
Lactate	May be raised	>2 mmol/L despite resuscitation
Mortality	Around 10%	Above 40%

Lactate is the most telling number. A rising lactate, even before the blood pressure goes, is the body telling you tissues aren’t getting enough oxygen and are running anaerobically. That’s the warning shot before frank shock arrives.

Why Catching It Early Matters So Much §

Every hour without antibiotics in septic shock is roughly a 7 to 8% increase in mortality. That single statistic is the reason for the order of operations in the steps above: blood cultures before antibiotics where possible, fluids running, MET called early rather than late.

The window for getting ahead of this is short. Once a patient tips into shock the recovery is long and ugly even when they survive it. The single most useful thing during the high-risk window after a biliary or abscess case is simply temperature trending in the first hour. If it spikes, it spikes fast, and the earlier the cluster of fluids, cultures, and antibiotics gets going, the better the patient does.

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Related §

• Liver Tumour Embolisation: TACE and SIRTEX both carry delayed septic risk from devitalised tumour tissue
• Genicular Artery Embolisation

Last updated May 11, 2026.