Related Experiment Video
Updated: Jul 3, 2026
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Severe Late-Onset Vitamin K Deficiency Bleeding Presenting With Subdural Hematoma and Seizures in a 4-Month-Old
Seyed Abdul Ahad Wadoodi1, Mohammad Masudi2,3, Ali Rahimi2,3
1Department of Internal Medicine, Faculty of Medicine, Herat University, Herat, Afghanistan.
Insights
Late-onset vitamin K deficiency bleeding (VKDB) can cause severe intracranial hemorrhage in infants, even after prophylaxis. Prompt diagnosis and vitamin K treatment are crucial for preventing severe outcomes.
Area of Science:
- Pediatrics
- Hematology
- Neonatology
Background:
- Vitamin K deficiency bleeding (VKDB) is a preventable cause of infant hemorrhage, particularly late-onset VKDB (2 weeks-6 months).
- Late-onset VKDB often presents as intracranial hemorrhage (ICH), potentially leading to death or long-term neurological damage.
- While neonatal vitamin K prophylaxis is effective, factors like infection can still contribute to late VKDB.
Purpose of the Study:
- To report a case of late-onset VKDB presenting with intracranial hemorrhage despite initial vitamin K prophylaxis.
- To highlight the importance of considering VKDB in infants with unexplained bleeding, especially after procedures or with concurrent infections.
- To emphasize the need for prompt diagnosis and management of VKDB to prevent severe sequelae.
Main Methods:
- A case report of a 4-month-old infant presenting with symptoms suggestive of sepsis and anemia.
- Investigation revealed an expanding hematoma post-intramuscular injection, leading to the discovery of profound coagulopathy.
- Diagnostic workup included coagulation studies, hemoglobin assessment, and neuroimaging.
Main Results:
- The infant developed a subdural hematoma and hypoxic-ischemic cerebral injury following an intramuscular injection, despite reported neonatal vitamin K prophylaxis.
- Coagulation studies confirmed severe coagulopathy, which improved with parenteral vitamin K administration.
- The infant experienced seizures and altered consciousness but recovered fully with intensive care, with no apparent neurological deficits at discharge.
Conclusions:
- This case underscores the possibility of late-onset VKDB presenting with severe intracranial hemorrhage, even with prior vitamin K prophylaxis.
- Clinicians must maintain a high index of suspicion for VKDB in infants with unusual bleeding, particularly when infections or minor procedures are involved.
- Early vitamin K therapy, coagulation assessment, and neuroimaging are vital for managing suspected VKDB and mitigating adverse outcomes.
Background:
Vitamin K deficiency bleeding (VKDB) remains a preventable cause of severe hemorrhage in early infancy. Late-onset VKDB (2 weeks-6 months) most commonly presents with intracranial hemorrhage (ICH) and can result in death or long-term neurological sequelae. Although routine neonatal intramuscular vitamin K prophylaxis is highly effective, late VKDB may still occur in the presence of contributing factors such as infection or impaired vitamin K availability.
Case Presentation:
A 4-month-old male infant presented with fever, cough, and poor appetite. He was delivered by cesarean section (birth weight 3200 g) and reportedly received 1-mg intramuscular vitamin K at birth. He was predominantly formula-fed with occasional breastfeeding and had no history of trauma or prior bleeding. Initial laboratory testing showed hemoglobin 9 g/dL and leukocytosis; sepsis with anemia was suspected, and intramuscular ceftriaxone was administered. Shortly after the first dose, he developed an expanding injection-site hematoma with active bleeding. Coagulation studies revealed profound coagulopathy (INR > 4, PT > 120 s, aPTT > 120 s), with a decline in hemoglobin to 6.3 g/dL. Parenteral vitamin K was given, leading to correction of coagulation parameters; however, seizures and deteriorating consciousness developed. Neuroimaging demonstrated a subdural hematoma with hypoxic-ischemic cerebral injury. The patient was managed in the intensive care unit with seizure control, blood transfusion, antimicrobial therapy, and supportive care. Seizures resolved and the neurological status returned to baseline. He was discharged after 10 days without apparent neurological deficits, with long-term neurodevelopmental follow-up advised.
Conclusions:
This case suggests probable late-onset VKDB presenting with life-threatening ICH despite reported neonatal vitamin K prophylaxis, while acknowledging that the complete exclusion of alternative causes of coagulopathy was limited by resource constraints. Clinicians should maintain a high index of suspicion for VKDB in infants with unexpected bleeding after minor procedures or intramuscular injections, particularly in the setting of intercurrent infection, and initiate prompt vitamin K therapy, coagulation assessment, and neuroimaging when indicated.
Related Concept Videos
01:24Disorders of Hemostasis
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
01:30Vitamins
01:29Hemorrhagic Stroke ll: Pathophysiology
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
01:17Hemorrhagic Stroke l: Introduction
01:30Venous Thrombosis IV: Nursing Management