Dr Muhammad Imran Ansari-ICU insights Pakistan

27/05/2026

Eid Mubarak everyone !

25/05/2026

Regarding my previous case, the answer to the summary is as follows.

24/05/2026

Patient: 35 y/o female
PMH: Asthma, non-compliant with medications
Presentation: Presented to ER with shortness of breath → progressed to respiratory distress requiring intubation.

Hospital Course:
1. Initial management: Treated for acute asthma exacerbation with inhalers, steroids, and ACS protocol. Initial troponin I was markedly elevated at 14,000 ng/L.
2. Cardiac evaluation: Initially managed conservatively for suspected ACS. Shock worsened. Repeat troponin rose to 45,000 ng/L. ECG showed ST elevation in I, aVL with reciprocal changes.
3. Coronary angiogram x2: Both showed non-obstructive coronaries, ruling out obstructive CAD/MI.
4. ICU course: Developed ventricular tachycardia → DCC shocks with intermittent CPR. Shock worsened despite support.
5. Further workup/treatment: Pulse steroid therapy for 3 days .

DD??

21/05/2026

Differential Diagnosis of my last patient case summary.

1 Meningoencephalitis - likely viral/aseptic

Why: 5-day history of headache + neck stiffness + rigidity, no fever mentioned but not ruled out. Normal LP and normal repeat CT don’t rule it out - early viral/aseptic meningitis can have normal CSF initially. The sudden deterioration could be due to cerebral edema, seizures, or sepsis.

The absence of fever, photophobia, and normal CSF makes bacterial meningitis less likely, but doesn’t exclude viral/aseptic causes.

2. PRES = Posterior Reversible Encephalopathy Syndrome

Why PRES could fit:
A Posterior circulation symptoms: Headache, altered mental status, seizures, visual disturbance. You have headache + neck stiffness + reduced GCS + seizure prophylaxis on board.
B Posterior circulation stroke on initial CT: PRES often affects posterior circulation territories and can be misread as infarct on non-contrast CT if there’s vasogenic edema.
C Triggers: PRES happens with severe HTN, eclampsia, sepsis, renal failure, immunosuppression. Our patient has HTN, DM, AKI with creat 3.2, and was in shock/sepsis-like state.
C Normal repeat CT: PRES lesions are often reversible and can resolve quickly on repeat imaging.

3 Posterior circulation stroke / Vertebrobasilar dissection

Why: “Severe neck pain” + neck stiffness + headache 5 days prior fits vertebrobasilar dissection or brainstem/cerebellar infarct. Initial CT reported posterior circulation stroke, though repeat CT was normal. Small brainstem infarcts can be missed on non-contrast CT. Dissection can cause neck pain + headache + posterior circulation ischemia.

4 Subarachnoid hemorrhage with vasospasm

5 CNS infection with rigidity - e.g. Tetanus or rabies.

What I’d push for next:
MRI brain + MRV/MRA

21/05/2026

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Critical Care Medicine

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20/05/2026

Case Summary
50-year-old male, known asthmatic since adolescence, on salbutamol/ipratropium inhalers/nebs PRN. Presented to other hospital ER with 5-day history of severe neck pain and worsening SOB, acutely deteriorated over hours.

Initial presentation at other hospital ER: GCS 15/15, BP 80/60 mmHg, HR 110, SpO2 60% on high-flow NRM.
Initial ABG: pH 7.37, pCO2 34, HCO3 16.6 → high anion gap metabolic acidosis with respiratory compensation.

In ER, sudden pulselessness, GCS drop, gasping → 1 cycle CPR, ROSC achieved. Emergency intubation done.
Post-arrest ABG: pH 6.93, pCO2 52, pO2 98, HCO3 8.8 → severe combined metabolic + respiratory acidosis.
Post-intubation GCS: 2/10.

Workup :
• CT Brain: Posterior circulation stroke initially, repeat CT normal.
• ECG: Deep T wave inversion. Trop I 6,000 → 8,000 ng/L.
• Echo: EF 25%, TAPSE 10 mm → severe LV dysfunction, RV dysfunction.
• LP: Normal CSF. ONSG normal.
• Labs: Hb 12.6, TLC 12.6, Plt 113. Creat 3.2 mg/dL. Na 159, K 3.6, Cl 117, Ca 7.9, Mg 2.4, Phos 4.7. INR 1.5. T.bili 0.3, SGOT 29, SGPT 127. CRP 16. Viral markers, Dengue NS1 negative.
• CXR: OAD pattern, bilateral infiltrates R>L, mid/lower zone predominance.
• Current: BP 110/60 on norad 0.15 mcg/kg/min + epi 0.05 mcg/kg/min. HR 88, SpO2 95% on FiO2 30%, GCS 7/10, urine output adequate.

Meds: Ceftriaxone, furosemide, levetiracetam, valproate, tramadol, clexane, aspirin + clopidogrel.

What are your differential diagnosis ??

18/05/2026

Our department recently hosted a discussion session with colleagues from infectious diseases, microbiology, anaesthesia, and cardiology to review the new sepsis guidelines.

17/05/2026

Clinical Case Summary

Patient Profile
60-year-old male with known HTN, DM, IHD admitted with Inferior Wall MI + Right Ventricular Infarction.

Coronary Anatomy & Intervention
• CAG: 3-vessel CAD
• Intervention: Successful PPCI to RCA. Attempted PCI to LCX was unsuccessful.

Hospital Course
• Initial Presentation: Admitted with IWMI + RVI.
• Deterioration: Stepped up from SDU to CCU. Intubated due to worsening acidosis.
• Echo: Biventricular dysfunction

Key Investigations

Arterial Blood Gas on Arrival to CCU- pre-intubation:
pH 7.28 / pCO₂ 19 mmHg / pO₂ 326 mmHg / HCO₃⁻ 8.8 mmol/L / SpO₂ 99% on FiO₂ 100%
Interpretation: Severe high anion gap metabolic acidosis with respiratory alkalosis. PaO₂ 326 on 100% FiO₂ confirms intubation/ventilation at time of sampling.

Arrival Labs:
• CBC: Hb 15 g/dL, TLC 15 ×10⁹/L, Platelets 152 ×10⁹/L
• RFTs: Creatinine 1.3 mg/dL
• Electrolytes: Na 128 mmol/L, K 4.4 mmol/L, Cl 93 mmol/L

Diagnosis & Reasoning

Primary Cardiac Diagnosis:
1. Inferior STEMI with RVI - confirmed by ECG, CAG, and clinical presentation.
2. 3-Vessel CAD - RCA stented successfully, LCX PCI failed.
3. Biventricular dysfunction post-MI.

Metabolic Diagnosis:
4. Diabetic Ketoacidosis (DKA) triggered by acute MI - not RV shock as initially suspected.

Evidence for DKA:
• Severe high anion gap metabolic acidosis: HCO₃⁻ 8.8, likely elevated anion gap.
• History of DM. Acute MI is a major stressor precipitating DKA.
• Respiratory compensation with low pCO₂ 19 mmHg.
• Hyponatremia Na 128 likely dilutional/pseudohyponatremia from hyperglycemia.

Why not RV shock alone?
RV infarction causes low CO, hypotension, elevated CVP, and typically lactic acidosis from hypoperfusion. Here, the acidosis was disproportionate, with HCO₃⁻ 8.8 and high AG, inconsistent with isolated RV failure. Clinical response to DKA management and temporal relation to MI supports DKA as primary drive.

16/05/2026

Answer of my patient case summary with differential diagnosis.

14/05/2026

Case Summary
29-year-old previously healthy male with 4-day history of fever + loose stools, presenting with high-grade fever, lethargy, sudden chest pain, hypotension, cold peripheries. Initially managed as ACS → transferred to cardiac tertiary hospital.Deteriorated with severe metabolic acidosis, respiratory distress → intubated.

Key findings:
• Hemodynamics: Shock on norepinephrine 0.2 µg/kg/min + vasopressin 0.04 U/min
• Cardiac: Troponin 17,251 ng/L, global LV dysfunction on echo .
• Hematology: Pancytopenia Hb 4.4 g/dL, TLC 3.4, Plt 57; high MCV, hemolysis in peripheral film,deranged liver functions .
• Respiratory: Hypoxic, pulmonary edema on CXR. Improved post-diuresis. Now FiO2 40%, PEEP 7
• Infectious: Viral hepatitis markers negative. B12 normal
• Cultures: Sent, pending
Pro calcitonin normal.

Differential Diagnosis?

14/05/2026

Critical care insights from Pakistan