Catastrophic consequences of prolonged immobilization after intracerebral hemorrhage: a case report of crush syndrome combined with capillary leak syndrome.

Background: Spontaneous intracerebral hemorrhage is a neurological emergency with high mortality and disability rates. Prolonged immobilization after stroke can trigger severe systemic complications. The simultaneous occurrence of crush syndrome and capillary leak syndrome in the setting of acute intracerebral hemorrhage is extremely rare and life-threatening, and no established treatment protocol exists. Case summary: A 64-year-old man with hypertension was found unconscious on his home floor. The estimated time from onset to discovery exceeded 24 h. He was diagnosed with left basal ganglia intracerebral hemorrhage of approximately 5.6 mL with intraventricular extension. On admission, he was comatose with a Glasgow Coma Scale score of 9. Systemic involvement was extensive: severe bilateral leg swelling with multiple tension bullae, acute kidney injury requiring continuous renal replacement therapy, severe rhabdomyolysis with a peak creatine kinase exceeding 50,000 U/L, hyperkalemia, with an initial arterial blood gas in the emergency department showing 6.9 mEq/L, elevated liver enzymes, and distributive shock. Admission central venous pressure was negative, strongly indicating severe hypovolemia. Chest CT already showed hypostatic pneumonia. The clinical presentation was consistent with crush syndrome from prolonged compression, which then led to secondary capillary leak syndrome. The patient underwent emergency neuroendoscopic hematoma evacuation and external ventricular drainage. Postoperatively, he developed atrial fibrillation and deep vein thrombosis. After 3 weeks of multidisciplinary intensive care, his liver and kidney function gradually improved, and the hypostatic pneumonia was controlled. He survived to discharge with a Glasgow Coma Scale score of 11, left limb muscle strength grade 3/5, and right limb muscle strength grade 0/5, and was transferred to a local hospital for continued rehabilitation. At 3-month follow-up, he was walking independently (mRS 2), with significant improvements in neurological function and quality of life. Conclusion: This case reveals a frequently overlooked but deadly clinical pathway: prolonged immobilization after intracerebral hemorrhage can lead to traumatic rhabdomyolysis, crush syndrome, and secondary capillary leak syndrome. A negative central venous pressure, a rare finding, provided supportive evidence of severe hypovolemia due to capillary leak syndrome. This clinical triad represents a unique high-risk condition that demands a shift in treatment philosophy from neurocentric care to systemic resuscitation.