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Inside the ICU, svc treewalk, Hyderabad (2025)

24/09/2025

A Challenging Case of STEC-HUS with Secondary Sepsis 🌟

Case summary:
73-year-old female admitted elsewhere with acute gastroenteritis, started on IV fluids and antibiotics. She deteriorated with shock, AKI requiring dialysis by day 3. Stool PCR confirmed STEC.

When shifted to our ICU:

Antibiotics stopped (no role in STEC initially).

Sepsis panel sent (negative).

Managed with fluids, dialysis started for worsening renal parameters.

Diagnosis: STEC-HUS (MAHA, AKI, but intact sensorium initially).

Neurological course:

On day 2 of dialysis, sensorium worsened, nystagmus noted.

EEG: metabolic encephalopathy.

CT brain: normal.

Progressed to GCS 3 → intubated.

Day 4: worsening TLC, shock, seizures (one GTCS), MRI: post-ictal changes.

Diagnostic dilemma:

Overlap STEC-HUS vs atypical HUS vs TTP considered.

Complements were high → atypical HUS less likely.

Planned plasma exchange but wanted to exclude secondary sepsis before proceeding.

Breakthrough:

Repeat sepsis panel + CSF: Stenotrophomonas maltophilia.

Treatment: Bactrim + Minocycline.

Course in ICU:

Continued dialysis (4 sessions total).

Shock resolved.

Sensorium improved.

No further seizures on AEDs.

Renal function recovered, dialysis stopped.

TLC & LFTs improved.

Extubated on day 8.

🔑 Clinical Pearls:

STEC-HUS: Antibiotics are usually avoided as they can worsen toxin release.

Atypical HUS: Consider if complements low/normal; in this case, complements were high, helping rule out.

TTP overlap: Always think of it when there’s MAHA + neurological worsening. Plasma exchange may be lifesaving—but rule out infection first.

Stenotrophomonas maltophilia: An opportunistic pathogen in critically ill/dialysis patients—early recognition and targeted therapy (Bactrim ± Minocycline) can be lifesaving.

EEG/MRI + CSF workup: Helped avoid unnecessary plasma exchange and directed therapy.

Multidisciplinary approach: Sequential thinking (HUS → atypical HUS → TTP → secondary sepsis) was key to survival in this complex case.

✅ Outcome: Patient improved, extubated, and recovering.
This case highlights the fine balance between timely immunomodulation and infection control in critically ill HUS patients.

23/09/2025

When Fever Isn’t Infection – A Case of PAN in the ICU

A 27-year-old man came with persistent fever and cough. He was managed outside as atypical pneumonia (suspected Mycoplasma), with multiple escalations – meropenem, levofloxacin, doxycycline – but fever never relented.

On day 10, low-dose steroids were given → fever resolved dramatically.
But within hours of discharge, he developed severe abdominal and testicular pain.

CT: only f***l load.

Doppler: reduced flow in hepatic and testicular arteries.

At our ICU:

Sepsis, IE, APLA workup done.

TEE negative, sepsis panel negative.

Started empiric antibiotics + heparin.

With infection ruled out, and steroids showing response, the suspicion turned to vasculitis.
We pulsed with high-dose steroids → dramatic improvement (pain, AKI, systemic symptoms).
Later, cyclophosphamide was added; ADA2 normal (DADA2 ruled out).
Final diagnosis: Polyarteritis Nodosa (PAN).

🔑 Clinical Pearls:

Persistent fever despite broad antibiotics → think non-infective causes.

Steroid responsiveness is a key clue to inflammatory/vasculitic illness.

PAN typically involves medium-sized arteries: renal, mesenteric, testicular, hepatic.

Always balance between sepsis vs vasculitis, especially when fever + systemic ischemic pain coexist.

✨ A young man walked in with “pneumonia” but walked out with a diagnosis that changed his life – PAN.

12/09/2025

Inside ICU: The Case of Lactate 22 Without Shock

She was only 55, a breast cancer warrior with lung metastases, and had been in and out of hospitals more times than she could count. This time she came in exhausted, struggling to breathe, her body frail, her spirit tired but unbroken.

On exam, she had severe pulmonary arterial hypertension (PAH) and clear signs of right heart failure—raised JVP, tender hepatomegaly, pedal edema. But something didn’t add up:

Blood pressure was stable, no signs of poor perfusion

No fever, no obvious infection

Yet her lactate was a staggering 22 mmol/L—a number that screams impending collapse in most patients.

🔍 The Hunt for a Cause:
We ran the gauntlet of investigations:

Sepsis? Cultures were negative, PCT 0.2, no inflammatory surge.

Pulmonary embolism? CT-PA pristine, Dopplers clean.

DKA? No ketones, sugars normal.

Renal failure? Creatinine steady, no AKI.

Left-sided HF? Echo confirmed severe PAH with RV dysfunction, preserved LV.

D-dimer: A jaw-dropping 35,000 ng/mL, but entirely explained by advanced malignancy.

Despite these terrifying labs, she wasn’t in shock. Something deeper was at play.

💡 Thinking Outside the Box:
High lactate without hypoxia or shock is Type B lactic acidosis.
She was cachectic, on chemo, with poor oral intake—a perfect setup for thiamine deficiency.

No time to wait for vitamin levels; we moved fast:

Thiamine 500 mg IV given immediately, then q8h × 3 doses.

⚡ The Turnaround:
Over the next 24 hours, magic unfolded:

Lactate plummeted from 22 → 2 mmol/L

Her alertness returned, breathing eased

No vasopressors, no invasive rescue measures—just a vitamin infusion

It was as if we had flipped a metabolic switch.

📌 Clinical Pearl:

“Not every lactate of 22 is sepsis. In oncology patients with cachexia and no shock, thiamine deficiency (Type B lactic acidosis) can masquerade as critical illness.
A low-cost vitamin, given empirically, can be the difference between decline and recovery.”

✨ Why This Matters:

Cancer patients burn through thiamine due to hypermetabolism

Chemotherapy, vomiting, and poor intake worsen deficiency

Type B lactic acidosis is often missed because we instinctively think “sepsis”

Recognizing this pattern can save lives with a simple intervention

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