Aryabhatta Sadhu/LinkedIn

Jul 3, 2026, 09:18

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.”

Aryabhatta Sadhu: Sickle Cell Crisis - When Diagnostics Should Change Therapy