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Inside the ICU, svc treewalk, Hyderabad (2025)

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

28/05/2025

Post-Liver Transplant ARDS – A Case of Courage, Collaboration, and Clinical Insight
This week in our ICU, we were reminded of how fragile the post-transplant journey can be—and how multidisciplinary decision-making can turn the tide even in the most complex situations.

👩‍⚕️ Case Snapshot:
A middle-aged woman underwent a live donor liver transplant for end-stage liver disease. Her immediate postoperative course was stable, and on Post-Op Day 1, she was awake, responsive, and hemodynamically steady in our ICU.

However, by Post-Op Day 2, she developed:

High-grade fever

Tachypnea and increased oxygen requirements

Bilateral infiltrates on chest imaging

ABG showing PaO₂/FiO₂ ratio < 120, confirming severe ARDS

🧠 Clinical Challenge:
The diagnosis of pneumonia-associated ARDS was clear—but the management was not.

Prone positioning, a proven strategy in severe ARDS (P/F < 150), was considered. However, her fresh abdominal incision, liver graft, and hepatic anastomosis raised major concerns about safety.

Would proning compromise the graft? Could it lead to anastomotic disruption or abdominal compartment issues?

🤝 The Multidisciplinary Approach:
We convened a rapid team huddle involving:

ICU physicians

Transplant surgeons

ICU nursing and respiratory therapy teams

After ensuring:

No signs of active bleeding or bile leak

Soft, non-tender abdomen

Stable hemodynamics

Satisfactory Doppler flow in the hepatic vasculature
..we received a green signal to prone her under close monitoring.

📈 Management Highlights:
Initiated proning sessions (16 hours/day) with full protective strategies for the surgical site

Started broad-spectrum antibiotics based on culture guidance

Continued lung-protective ventilation (low tidal volume, moderate PEEP)

Maintained close monitoring of abdominal girth, drain outputs, and hemodynamics

Within 48 hours of prone ventilation:

P/F ratio improved from 180

FiO₂ requirements decreased

Lung compliance improved

Over the next 4–5 days, she continued to recover, and was:

Extubated on Day 7 post-transplant

Transferred to step-down by Day 10

Discharged home in stable condition

🩻 Clinical Pearls:
🔹 Prone positioning can be safely performed in post-liver transplant patients if:

The abdominal wound is intact

There are no signs of graft dysfunction or vascular compromise

Surgical clearance is obtained

🔹 Early multidisciplinary input is critical in high-stakes cases. Quick coordination can help implement lifesaving interventions without unnecessary delay.

🔹 Always monitor drain outputs, abdominal pressures, and Doppler flows in transplant patients undergoing prone sessions.

🔹 Don’t allow historical caution to override emerging evidence. When done right, proning is not just safe—it’s lifesaving.

💬 Final Thought:
This case was a powerful reminder that even the most fragile post-op patients can benefit from aggressive yet thoughtful ICU strategies. Science, teamwork, and courage—this is what critical care is all about.

26/05/2025

A Storm of Clots – The Silent Fury of Catastrophic APLA

She was 68—diabetic, hypertensive—brought in with a swollen, painful right leg. What started as a presumed peripheral vascular disease quickly took a devastating turn. Within hours, her limb turned cold and dusky, rapidly evolving into above-knee gangrene.

Initial labs revealed acute kidney injury, rising lactate, and leukocytosis. As she spiraled into metabolic acidosis and hypotension, we shifted her to our ICU.

On arrival: tachypnea, tachycardia, bilateral crackles, and hypoxia. Bedside echo showed regional wall motion abnormality and pulmonary edema. She was intubated immediately.

Her husband and daughter sat quietly beside her stretcher, eyes filled with questions they didn’t know how to ask.
“Is this something we can treat?” her daughter finally whispered.

We explained: this was not routine sepsis or simple vascular occlusion. Her blood work showed thrombocytopenia, elevated D-dimer, aPTT prolongation, and LDH surge. Doppler confirmed both arterial and venous thrombosis of the right lower limb. Antiphospholipid antibody panel returned strongly positive for lupus anticoagulant and anti-β2 glycoprotein I antibodies.

The diagnosis: Catastrophic Antiphospholipid Antibody Syndrome (CAPS) — a rare, fulminant, autoimmune condition that causes widespread, rapid clot formation across multiple organs.

Management Strategy:

Full anticoagulation with IV heparin

Pulse methylprednisolone

Plasmapheresis, initiated within 6 hours of diagnosis

Broad-spectrum antibiotics

Organ support: mechanical ventilation, vasopressors, and CRRT

Despite aggressive therapy, ischemia progressed. After discussion with the vascular team and family, we proceeded with above-knee amputation to control the source and limit systemic inflammatory response.

Her family was devastated, but resilient. “Save her life. We’ll manage the rest,” her husband said quietly.

Over the next few days, we witnessed slow recovery:

Renal function improved.

She came off vasopressors.

We weaned her off the ventilator.

She fought hard, and with a coordinated ICU-rheumatology-vascular-nephrology effort, she pulled through.

Clinical Pearls from the Case:

Always suspect CAPS in patients with multi-organ dysfunction and both venous and arterial thromboses.

CAPS is a diagnosis of speed—delayed recognition costs lives.

Triple therapy (heparin + steroids + plasma exchange or IVIG) remains the cornerstone.

Multidisciplinary care saves lives—rheumatology, intensivists, nephrology, hematology, and surgeons must work as one.

Antiphospholipid Syndrome isn’t always chronic—CAPS is its most aggressive form and often the first manifestation.

She is alive today—with one less limb but a renewed life—thanks to vigilance, timely decisions, and relentless care. And above all, the strength of a husband and daughter who stood by her without wavering.

Inside the ICU, sometimes we don’t just fight disease—we fight time, systems, and fate.

25/05/2025

The Danger Beneath – A Case of NOMI

Post-op Day 2 after TKR – Everything looked routine… until it wasn’t.

Our patient, a 68-year-old post-total knee replacement, was recovering well — until subtle abdominal distension crept in. No peritonitis, no guarding, just vague fullness. A CECT abdomen showed ileus. Conservative management began. But the patient’s clinical course told another story.

Over 24 hours — worsening shock, AKI, increasing pressor requirements, and eventual intubation. Repeat CECT abdomen showed no obvious occlusion, with “normal” appearing mesenteric vessels and only subtle bowel changes. Too subtle.

Something didn’t add up. The numbers, the exam, the deteriorating trajectory — all were screaming beneath the surface. Despite no classical signs, we pressed for a diagnostic laparoscopy.

And there it was – patchy small bowel necrosis. Diagnosis: Non-Obstructive Mesenteric Ischemia (NOMI).

Takeaway for budding intensivists:
NOMI doesn’t always announce itself with textbook findings. When the gut is sick, but scans are “normal,” trust the trajectory. In the ICU, deterioration despite supportive care is the biggest red flag. Imaging may lag behind clinical truth.

Push for the laparoscopy when the gut whispers, not just when it screams.

Clinical Pearls:

NOMI often presents with vague abdominal signs and rapid clinical decline — not always dramatic imaging.

Normal mesenteric vessels on imaging don’t rule out ischemia. Look for bowel wall thinning, lack of enhancement, or unexplained ileus.

Always correlate imaging with the clinical picture. A “normal” scan can mislead in evolving ischemia.

In post-op or vasopressor-dependent patients, maintain a high index of suspicion for NOMI if shock worsens without clear cause.

Laparoscopy can be both diagnostic and life-saving — escalate when deterioration outpaces diagnostics.

23/05/2025

Hyperacute Liver Failure in a Young Female – A Case Reflection

Case Overview:

We recently managed a 26-year-old female referred to our ICU from Bhopal with a diagnosis of acute viral hepatitis A, complicated by hyperacute liver failure. The presentation was abrupt, with rapid deterioration over a few days marked by coagulopathy, hepatic encephalopathy, rising transaminases, and progressive hemodynamic instability.

Initial Stabilization:

On arrival, the patient was hypotensive, encephalopathic (Grade II), and in early acute kidney injury. Resuscitation was initiated per standard protocol — cautious fluid management, vasopressor support, N-acetylcysteine infusion, and empirical antibiotics. A high index of suspicion was maintained for sepsis and worsening hepatic insult.

Decision for Transplant:

Given the rapid deterioration and King’s College Criteria being fulfilled, an emergency transplant was the only viable option. After thorough counseling, her brother was evaluated and accepted as a suitable living donor. The transplant was completed successfully within 48 hours of ICU admission.

Post-Transplant Course:

The immediate postoperative course was complicated by:

Ventilator-associated pneumonia (VAP) on Day 4

Prolonged mechanical ventilation with sedation and neuromuscular blockade

Liver graft function monitoring with LFT trends, Doppler studies, and immunosuppressive drug levels

Sepsis surveillance and antifungal coverage, considering high-risk immunosuppressed status

She gradually improved, was weaned off vasopressors, and extubated on Day 18. Intensive physiotherapy, nutritional rehabilitation, and close graft monitoring continued.

Outcome:
After 28 days in ICU, the patient was discharged to the ward in stable condition, with good graft function and no neurological sequelae.

Key Teaching Points...

Recognize fulminant liver failure early — timely referral and transplant listing are crucial.

King’s College Criteria remain a valuable guide for transplant decision-making in acute liver failure.

ICU management post-liver transplant requires:

A balance between immunosuppression and infection control

Vigilant monitoring for VAP and multi-drug resistant organisms

Supportive care targeting hepatic, renal, and respiratory systems

Multidisciplinary coordination between intensivists, transplant surgeons, hepatologists, and infectious disease specialists is vital for outcomes.

This case was a powerful reminder of how prompt diagnosis, decisive intervention, and critical care teamwork can rewrite a prognosis. As young intensivists, stay sharp, act fast, and never underestimate the value of timely conversations with families.

21/05/2025

Super-Refractory Status Epilepticus in a Pregnant Young Woman – A War Fought on Two Fronts

Patient Profile:

26-year-old primigravida, 22 weeks gestation, previously healthy, was referred to our ICU in super-refractory status epilepticus (SRSE) – seizures unresponsive to multiple antiepileptic drugs and anesthetics.

Initial Presentation

She developed new-onset generalized tonic-clonic seizures, rapidly escalating into status epilepticus. Despite treatment with IV lorazepam, levetiracetam, valproate, and midazolam infusion, seizures persisted. She was intubated, loaded with phenytoin and thiopentone, and transferred to our center in pharmacologic coma.

On ICU Admission:

GCS: E1VTM1

EEG: Persistent epileptiform discharges, no effective burst suppression

Fetal heart: Present with reactive trace initially

Hemodynamics: Stable, on minimal vasopressors

Diagnosis: SRSE, suspected autoimmune/unknown etiology

Comprehensive Multimodal Management:

AEDs: Levetiracetam, valproate, phenytoin, lacosamide, perampanel

Anaesthetics: Midazolam, thiopentone, ketamine, and propofol (rotated)

Immunotherapy:

IV Methylprednisolone 1g x 5 days

IVIG 2g/kg over 5 days

Autoimmune panel: ANA positive; anti-NMDA negative

CSF: Lymphocytic pleocytosis; infectious panel negative

MRI Brain: Unremarkable

Support: Tight glycemic control, DVT prophylaxis, enteral feeding

Critical Decision – Tracheostomy & Obstetric Intervention:

Due to prolonged ventilation, tracheostomy was done on ICU Day 10.

Seizure activity remained uncontrolled despite maximal therapy.

After extensive multidisciplinary consultation, including neurology, critical care, obstetrics, and ethics, pregnancy was medically terminated in view of persistent maternal instability and poor fetal prognosis.

Game-Changer – Electroconvulsive Therapy (ECT):

Three sessions of ECT were given under controlled sedation. Remarkable EEG and clinical improvement noted post-session 2. Seizures ceased, sedation weaned off gradually over one week.

Recovery Phase:

EEG normalized

AEDs tapered to maintenance with levetiracetam, lacosamide, clobazam

Gradual neurological improvement, no focal deficits

Tracheostomy decannulated before ICU discharge

Transferred to step-down neuro-rehabilitation

Reflections:

SRSE during pregnancy is a rare, high-stakes condition requiring aggressive, multi-pronged management

ECT can be a life-saving rescue therapy

Maternal life must remain the central focus when fetal compromise is inevitable

Emotional toll and ethical complexity are profound – holistic, team-based care is vital

Outcome:

Mother discharged neurologically intact

Pregnancy outcome: terminated for maternal survival

Long-term follow-up planned with neurology and psychiatry

This was not just a clinical battle – it was an emotional, ethical, and human journey. The ICU remains a place where decisions are made not just with data, but with heart and courage.

18/05/2025

Inside the ICU: A Case That Made Us Pause

We admitted a 32-year-old male to our ICU with severe breathlessness. He had no previous medical conditions, no history of smoking, and led an active lifestyle. When he arrived, his oxygen saturation was critically low despite high-flow oxygen. He was intubated within the first hour.

Initial investigations were inconclusive.

Chest X-ray: Clear

ECG: Normal

No fever, no signs of infection

COVID and other viral panels: Negative

CTPA: No pulmonary embolism

CT chest showed bilateral ground-glass opacities, which raised the possibility of interstitial or inflammatory lung disease. It didn’t look like classic ARDS. We were puzzled.

While taking a more detailed history, his wife mentioned he had recently started using a new essential oil spray in a closed, air-conditioned room every night. This was an important clue.

We suspected hypersensitivity pneumonitis or toxic inhalational injury. A bronchoalveolar lavage was done, which revealed hemosiderin-laden macrophages and eosinophilic infiltrates — consistent with alveolar hemorrhage due to inhalation exposure.

He was started on high-dose steroids and gradually improved over the next few days. He was successfully extubated and later discharged with full recovery.

Challenges in this case:

- The patient couldn’t give history due to respiratory failure

- There were no obvious triggers

- Radiology findings were nonspecific

- The crucial exposure history came only through detailed questioning

Sometimes, it’s not about complex diseases — it’s about simple things we overlook, like a room spray in a closed space. This case reminded us of the importance of thorough history-taking and thinking beyond the obvious.

17/05/2025

ALL ABOUT ECMO — A COMPLETE GUIDE FOR BUDDING INTENSIVISTS
By Inside the ICU

In the ever-evolving field of critical care, ECMO (Extracorporeal Membrane Oxygenation) is one of the most advanced and demanding life support strategies we use. For young intensivists, understanding ECMO is not just about knowing the machine — it's about mastering clinical judgment, timing, teamwork, and ethical decision-making.

What is ECMO?
At its core, ECMO is an artificial heart-lung support system. It temporarily takes over the function of one or both organs:

Oxygenates blood

Removes carbon dioxide

Supports cardiac output (in certain cases)

It allows the lungs and/or heart to rest and recover.

Types of ECMO

Veno-Venous (VV ECMO)

Purpose: Lung support only

Indications: Severe ARDS, viral pneumonia (COVID-19), aspiration, trauma

Access: Venous drainage and return (usually femoral + internal jugular)

Heart must be functionally adequate

Veno-Arterial (VA ECMO)

Purpose: Cardiac ± lung support

Indications: Cardiogenic shock, fulminant myocarditis, cardiac arrest (ECPR), post-cardiotomy shock

Access: Venous drainage, arterial return (femoral or central cannulation)

Higher risk profile than VV

When to Consider ECMO?

ECMO is NOT a first-line therapy. It comes into the picture when:

Mechanical ventilation and medical management fail.

There is a potentially reversible cause.

The patient is failing oxygenation/ventilation (PaO₂/FiO₂ < 80 despite optimal PEEP).

Cardiac output is inadequate despite vasopressors and inotropes.

The patient has no absolute contraindications (e.g., severe brain injury, metastatic malignancy).

Early referral to an ECMO-capable center improves survival.

Key Components of ECMO Management
Patient Selection

This is the most critical step.

Evaluate reversibility, comorbidities, pre-ECMO organ function, and goals of care.

Cannulation Technique

Percutaneous vs surgical

Ultrasound and fluoroscopic guidance are ideal

Must ensure proper positioning and secure fixation

Circuit Management

Monitor for oxygenator failure, clot formation, flow issues

Regular checks for hemolysis, infections, and circuit integrity

Anticoagulation

Unfractionated heparin is most commonly used

Monitor ACT or anti-Xa levels regularly

Balance bleeding vs clotting risk

Multidisciplinary Team Approach

Intensivist, perfusionist, critical care nurses, respiratory therapist, physiotherapist, cardiologist, surgeon

Communication is key to outcomes

Common Complications
Bleeding (due to anticoagulation and circuit trauma)

Thrombosis (circuit or patient-side)

Infections

Limb ischemia (especially in peripheral VA ECMO)

Neurological injury

Mechanical failure of the circuit

Weaning & Decannulation
VV ECMO: Wean as lung compliance improves and gas exchange stabilizes

VA ECMO: Requires comprehensive cardiac assessment — echocardiography, lactate clearance, pulsatility

Trial off support is done with close hemodynamic and ABG monitoring

Ethical Considerations
ECMO can prolong dying, not just life.

Discuss goals of care early with families.

Involve palliative care when appropriate.

“ECMO should be offered with clarity, not as a reflex.”

Final Thoughts for Budding Intensivists
ECMO is not glamorous — it's complex, exhausting, and demanding.

You need sound clinical acumen, not just textbook knowledge.

Know when to say no — futile ECMO is worse than no ECMO.

Learn from each case — successes and failures alike.

"The ventilator supports the lungs. ECMO supports the clinician’s hope — but only when used wisely."

Stay sharp. Stay compassionate. And never stop learning.

17/05/2025

Welcome to INSIDE THE ICU!

As a critical care specialist, I’ve spent countless hours by the bedside, managing ventilators, ECMO circuits, and the fragile balance of life in the ICU.

This page is my attempt to share practical knowledge, clinical tips, and real-world experiences from the world of critical care — for students, colleagues, and anyone who wants to understand what goes on behind those ICU doors.

Follow along for:

ICU insights and case-based learning

Ventilator and ECMO pearls

Evidence-based practices simplified

Reflections from the frontline

Let’s make critical care more accessible, one post at a time.
Feel free to share, comment, and ask questions.

Inside the ICU

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