Aryabhatta Sadhu: Sickle Cell Crisis – When Diagnostics Should Change Therapy
Aryabhatta Sadhu, Attending Consultant and Head of Transfusion Medicine at Fortis Hospital Shalimar Bagh, New Delhi, 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.
-
Aug 13, 2026, 11:15Bridging Neurology and Thrombosis: Key Priorities from a New Expert Consensus Report – International Journal of Stroke
-
Aug 13, 2026, 11:05Khaled Musallam: The Evolving Landscape of β-Thalassemia: Clinical Trial Advances Since 2021
-
Aug 13, 2026, 10:31Brad Wilson: Clinical Insights from the Landmark ESC 2026 Trials
-
Aug 13, 2026, 10:23Rania Baleela: Evaluating Bedside Diagnostics and VICC Outcomes in Hemotoxic Snakebite
-
Aug 13, 2026, 10:11Christina Kounoudi: Low-Dose vs. Therapeutic Anticoagulation in Extended VTE Prophylaxis
-
Aug 13, 2026, 10:10Jean Connors: Can Prothrombin Levels Improve Antiphospholipid Syndrome Risk Assessment?
-
Aug 13, 2026, 09:44Edward Lee Carter: Why Clinically Relevant Nonmajor Bleeding Demands Anticoagulation Stewardship?
-
Aug 13, 2026, 09:40Neel Bhut: Can AI Help Us Make Gene Therapy More Efficient?
-
Aug 13, 2026, 08:23Sally Mandour: The Diagnostic Challenge of Hypocellular Bone Marrow Failure