Aryabhatta Sadhu: Sickle Cell Crisis – When Diagnostics Should Change Therapy
Aryabhatta Sadhu, Senior Resident Doctor at AIIMS, shared a post on LinkedIn:
“The Dangerous Turn in Sickle Cell Crisis: Detect Early, Exchange Fast
Sickle cell crisis is not one clinical event.
It is a spectrum – from uncomplicated vaso-occlusive pain to acute chest syndrome, stroke, fat embolism syndrome, and multiorgan failure.
The real decision point is identifying when diagnostics should change therapy.
This infographic maps a practical escalation pathway for severe sickling crisis, focusing on:
- Early warning signs of impending complicated crisis
- Diagnostic triggers separating uncomplicated VOC from organ-threatening disease
- When simple transfusion may be sufficient
- When urgent red cell exchange is required
- Where high-volume / sequential plasma exchange may fit as rescue adjunct therapy in refractory multiorgan failure or fat embolism syndrome
Hard decision points for HbS% tracking:
- In uncomplicated VOC, HbS% alone should not trigger transfusion. Clinical deterioration matters more.
- In ACS, neurologic symptoms, falling SpO₂, progressive infiltrates, organ dysfunction, or suspected fat embolism syndrome – send HbS% early and activate transfusion/apheresis planning.
- In severe ACS, acute stroke, multiorgan failure, or suspected FES – do not wait for HbS% to return if the patient is clinically deteriorating. Start urgent red cell exchange planning.
- Post-RCE target: HbS less than or equal to 30%, with hemoglobin generally kept around 10–11 g/dL to avoid hyperviscosity.
- Persistent HbS more than 30% after RCE, or rebound HbS with worsening hypoxemia, encephalopathy, thrombocytopenia, rising LDH/bilirubin/creatinine, should trigger repeat clinical review, repeat HbS quantification, and consideration of further exchange or adjunct PLEX in expert settings.
The key point is simple:
Do not transfuse reflexively for uncomplicated pain crisis.
Do not delay exchange when hypoxemia, neurologic decline, organ failure, or fat embolism physiology appears.”

Other posts featuring Aryabhatta Sadhu with Hemsotasis Today.
-
Jul 3, 2026, 09:33Abdul Mannan: Not All Type 1 VWD Starts in the VWF Gene
-
Jul 3, 2026, 05:55New Evidence Supports Chromogenic Assays After Hemophilia A Gene Therapy – JTH
-
Jul 3, 2026, 05:50Jacopo Parizzi: Roche’s Non-Malignant Hematology Team Is Looking Ahead to 2027
-
Jul 3, 2026, 05:25Brian A Beh: A New Approach from The George Institute for Global Health Could Transform Stroke Care Before Hospital Arrival
-
Jul 3, 2026, 05:22Deirdre Finnigan: New Insights into Red Blood Cell Biomechanics in Cancer-Associated Anemia
-
Jul 3, 2026, 05:15Danielle Boyle: Collaboration Across Borders Is Helping Shape the Future of ITP Care
-
Jul 3, 2026, 05:05Claire McIvor: One Year at the Stroke Association and Grateful for a Workplace That Made It Possible
-
Jul 2, 2026, 23:11Michael Makris: Join The Cancer Associated Thrombosis Workshop at ISTH 2026
-
Jul 2, 2026, 21:54Rob Maloney: Rare Disease Requires Relational Care